Materiały źródłowe

• #1 Mechanism of poisoning – WikiLectures

  https://www.wikilectures.eu/w/Mechanism_of_poisoning

  A poison is a substance that, when administered in small amounts, causes pathological changes or even death due to its chemical properties. Poisons act in the body through various mechanisms: […] Highly reactive aldehydes are examples of these poisons. The aldehyde group -CHO reacts readily with the amino group -NH2 or the sulfhydryl group -SH, which is abundant in proteins. An example is methanal (formaldehyde, HCHO). Its aqueous saturated solution is known as formalin. […] Some poisons disturb the acid-base balance of the organism. Ethylene glycol is oxidized by alcohol dehydrogenase to glycolic, glyoxal, and oxalic acids, which cause metabolic acidosis. Salicylates stimulate the respiratory center. The resulting hyperventilation leads to respiratory alkalosis. After entering the cells, they disrupt oxidative phosphorylation in the mitochondria, reduce ATP production, block citrate cycle enzymes, and stimulate anaerobic glycolysis. The result is the overproduction and accumulation of acidic metabolites, mainly lactate, pyruvate, and acetoacetate, and thus the development of metabolic acidosis.

• #1 Mechanisms of Toxicity

  https://www.iloencyclopaedia.org/part-iv-66769/toxicology-57951/mechanisms-of-toxicity

  Mechanistic toxicology is the study of how chemical or physical agents interact with living organisms to cause toxicity. […] Knowledge of the mechanism of toxicity of a substance enhances the ability to prevent toxicity and design more desirable chemicals; it constitutes the basis for therapy upon overexposure, and frequently enables a further understanding of fundamental biological processes. […] Understanding the mechanism by which a substance causes toxicity enhances different areas of toxicology in different ways. […] Mechanistic understanding helps the governmental regulator to establish legally binding safe limits for human exposure. […] If the mechanism of toxicity is understood, descriptive toxicology becomes useful in predicting the toxic effects of related chemicals. […] Understanding mechanisms of toxicity is the art and science of observation, creativity in the selection of techniques to test various hypotheses, and innovative integration of signs and symptoms into a causal relationship.

• #1 Mechanism and Health Effects of Heavy Metal Toxicity in Humans | IntechOpen

  https://www.intechopen.com/chapters/64762

  Several heavy metals are found naturally in the earth crust and are exploited for various industrial and economic purposes. […] The focus of this chapter is to describe the various mechanism of intoxication of some selected heavy metals in humans along with their health effects. Therefore it aims to highlight on biochemical mechanisms of heavy metal intoxication which involves binding to proteins and enzymes, altering their activity and causing damage. […] The mechanism by which heavy metals cause neurotoxicity, generate free radical which promotes oxidative stress damaging lipids, proteins and DNA molecules and how these free radicals propagate carcinogenesis are discussed. […] In the human body, these heavy metals are transported and compartmentalized into body cells and tissues binding to proteins, nucleic acids destroying these macromolecules and disrupting their cellular functions.

• #1 Mechanism and Health Effects of Heavy Metal Toxicity in Humans | IntechOpen

  https://www.intechopen.com/chapters/64762

  Heavy metal-bound proteins may be a substrate for certain enzymes. In such situations, the heavy metal-bound protein fits into an enzyme in a highly specific pattern to form an enzyme-substrate complex and thus cannot accommodate any other substrate until it is freed. […] Heavy metals may also inhibit protein folding. […] Heavy metal may cause proteins to aggregate as arsenite-induced protein aggregation was observed and shown to be concentration-dependent. […] Heavy metal-induced carcinogenesis includes epigenetic alterations, damage to the dynamic DNA maintenance system and generation of ROS. […] The mechanism of lead-induced carcinogenic process is postulated to induce DNA damage, disrupt DNA repair system and cellular tumor regulatory genes through the generation of ROS. […] The proposed mechanism of mercury-induced cancer is through the generation of free radicals inducing oxidative stress thereby damaging biomolecules.

• #1 Mechanism and Health Effects of Heavy Metal Toxicity in Humans | IntechOpen

  https://www.intechopen.com/chapters/64762

  As such, heavy metal toxicity can have several consequences in the human body. It can affect the central nervous function leading to mental disorder, damage the blood constituents and may damage the lungs, liver, kidneys and other vital organs promoting several disease conditions. […] The various mechanisms that lead to heavy metal toxicity with emphasis on macromolecule and cellular damages, carcinogenesis, neurotoxicity and the molecular basis for their noxious effects. […] The mechanism of free radical generation is specific to the type of heavy metal. […] The main mechanism of heavy metal toxicity include the generation of free radicals to cause oxidative stress, damage of biological molecules such as enzymes, proteins, lipids, and nucleic acids, damage of DNA which is key to carcinogenesis as well as neurotoxicity.

• #1 Mechanism and Health Effects of Heavy Metal Toxicity in Humans | IntechOpen

  https://www.intechopen.com/chapters/64762

  Nickel has an extensive range of carcinogenic mechanisms which include regulation of transcription factors, controlled expression of certain genes and generation of free radicals. […] Some heavy metals such as lead and manganese may affect the brain and cause neurological toxicity. […] Lead can impair learning and memory in the brain by inhibiting the N-methyl-d-aspartate receptor (NMDAR) and can block neurotransmission by inhibit neurotransmitter release, block the neuronal voltage-gated calcium (Ca2+) channels (VGCCs) and reduce the expression of brain-derived neurotrophic factor (BDNF). […] Manganese is known to accumulate in the mitochondria of neurons, astrocytes and oligodendrocytes cells and disrupts ATP synthesis by inhibiting the F1/F0 ATP synthase or complex 1 (NADH dehydrogenase) of the mitochondrial respiration chain. […] The disruption of ATP synthesis by manganese leads to decreased intracellular ATP levels and generation of free radicals thereby increasing oxidative stress which may contribute to manganese cellular toxicity.

• #1 Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5363978/

  Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. […] The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. […] CO binds to hemoglobin (Hb) in the blood with high affinity, forming COHb. […] CO binding to Hb also stabilizes the relaxed, high-affinity quaternary state of Hb (known as R-state), increasing the affinity for oxygen of other sites within the Hb tetramer, and further reducing oxygen release and delivery. […] CO inhibits mitochondrial respiration by binding the ferrous heme a3 in the active site of COX, effectively shutting down oxidative phosphorylation, similar to the effects of cyanide and nitric oxide (NO).

• #1 Poisoning – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/poisoning/

  Cyanide blocks the electron transport chain by binding to cytochrome complex IV oxidative phosphorylation anaerobic metabolism, lactic acid, histotoxic hypoxia. […] Cyanide poisoning is primarily a clinical diagnosis. […] Cyanide poisoning is primarily a clinical diagnosis. […] Do not delay empiric antidotal treatment if cyanide poisoning is suspected. […] Hydroxocobalamin is the first-line antidote for cyanide poisoning. […] Nitrites induce methemoglobinemia by oxidizing hemoglobin to create methemoglobin. […] Sodium thiosulfate supplies sulfur donors to the mitochondrial enzyme rhodanese.

• #1 Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5363978/

  CO-mediated reductions in oxygen delivery and mitochondrial oxidative phosphorylation produce ischemic and anoxic brain injury, leading to cognitive deficits in survivors. […] The pathophysiology of CO poisoning involves the reduction of global oxygen delivery and the inhibition of mitochondrial respiration. […] The inflammatory cascade driven by NO and ROS contributes to neurological and cardiac injuries from CO poisoning. […] CO-induced mitochondrial inhibition could cause a stunned myocardium-like syndrome (with hypokinesia in the setting of unobstructed coronary arteries).

• #1 Organophosphate Toxicity: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/167726-overview

  Organophosphate toxicity is a clinical diagnosis. Confirmation of organophosphate poisoning is based on the measurement of cholinesterase activity; but typically, these results are not readily available. […] The primary mechanism of action of organophosphate pesticides is inhibition of carboxyl ester hydrolases, particularly acetylcholinesterase (AChE). AChE is an enzyme that degrades the neurotransmitter acetylcholine (ACh) into choline and acetic acid. […] Organophosphates inactivate AChE by phosphorylating the serine hydroxyl group located at the active site of AChE. Over a period of time, phosphorylation is followed by loss of an organophosphate leaving group and the bond with AChE becomes irreversible, a process known as aging. […] Once AChE has been inactivated, ACh accumulates throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic receptors. Clinical effects are manifested via activation of the autonomic and central nervous systems and at nicotinic receptors on skeletal muscle. […] Organophosphates can be absorbed cutaneously, ingested, inhaled, or injected. Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure, and rate of metabolic degradation.

• #1 Organophosphate poisoning – Wikipedia

  https://en.wikipedia.org/wiki/Organophosphate_poisoning

  Organophosphate poisoning is poisoning due to organophosphates (OPs). Organophosphates are used as insecticides, medications, and nerve agents. […] The underlying mechanism involves the inhibition of acetylcholinesterase (AChE), leading to the buildup of acetylcholine (ACh) in the body. […] The health effects associated with organophosphate poisoning are a result of excess acetylcholine (ACh) present at different nerve synapses and neuromuscular junctions across the body. Specifically, acetylcholinesterase (AChE), the enzyme that normally and constantly breaks down acetylcholine, is inhibited by the organophosphate substance. ACh accumulates in the parasympathetic nervous system, the central nervous system, and in nicotinic neuromuscular junctions. […] Organophosphate inhibition of AChE may be reversible or irreversible, depending on whether covalent bonding (also called „aging” in this context) occurs. […] Chemically, organophosphates cause poisoning by phosphorylating the serine hydroxyl residue on AChE, which inactivates AChE. This causes disturbances across the cholinergic synapses and can only be reactivated very slowly, if at all.

• #1 Cyanide poisoning – Wikipedia

  https://en.wikipedia.org/wiki/Cyanide_poisoning

  Cyanide is a potent cytochrome c oxidase (COX, a.k.a. Complex IV) inhibitor, causing asphyxiation of cells. As such, cyanide poisoning is a form of histotoxic hypoxia, because it interferes with the ability of cells to take or use oxygen via oxidative phosphorylation. […] Specifically, cyanide binds to the heme a3-CuB binuclear center of COX (and thus is a non-competitive inhibitor of it). This prevents electrons passing through COX from being transferred to O2, which not only blocks the mitochondrial electron transport chain, it also interferes with the pumping of a proton out of the mitochondrial matrix which would otherwise occur at this stage. Therefore, cyanide interferes not only with aerobic respiration but also with the ATP synthesis pathway it facilitates, owing to the close relationship between those two processes.

• #1

  https://link.springer.com/article/10.1007/s13181-019-00710-5

  Hydrogen sulfide (H2S) is found in various settings. […] In this paper we performed a review of the available literature on the mechanism of toxicity, clinical presentation, and development of countermeasures for H2S toxicity. […] In vivo, H2S undergoes an incomplete oxidation after an exposure. The remaining non-oxidized H2S is found in dissolved and combined forms. […] The combined non-soluble forms are found as acid-labile sulfides and sulfhydrated proteins, which play a role in toxicity. […] Recent countermeasure development takes into account the toxicokinetics of H2S. […] Some countermeasures focus on binding free hydrogen sulfide (hydroxocobalamin, cobinamide); some have direct effects on the mitochondria (methylene blue), while others work by mitigating end organ damage by generating other substances such as nitric oxide (NaNO2).

• #1 Arsenic exposure and chronic poisoning – UpToDate

  https://www.uptodate.com/contents/arsenic-exposure-and-chronic-poisoning

  Arsenic toxicity can vary greatly depending on the chronicity and dose of exposure and the chemical properties of the arsenical compound (eg, valence, complexed structures). […] Arsenic exposure can be asymptomatic or cause skin changes, hepatotoxicity, cardiovascular effects (eg, dysrhythmias), sensorimotor neuropathy, and diabetes mellitus. […] Latent or long-term effects of arsenic exposure include an increased risk of cancers, even after exposure has ceased.

• #1 Food Poisoning: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/175569-overview

  Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The pathogenesis of diarrhea in food poisoning is classified broadly into either noninflammatory or inflammatory types. Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory mechanisms of the mucosa of the small intestine, without invasion. This leads to large volume watery stools in the absence of blood, pus, or severe abdominal pain. Occasionally, profound dehydration may result. The enterotoxins may be either preformed before ingestion or produced in the gut after ingestion. Examples include Vibrio cholerae, enterotoxic Escherichia coli, Clostridium perfringens, Bacillus cereus, Staphylococcus organisms, Giardia lamblia, Cryptosporidium, rotavirus, norovirus, and adenovirus.

• #1 Food Poisoning: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/175569-overview

  Inflammatory diarrhea is caused by the action of cytotoxins on the mucosa, leading to invasion and destruction. The colon or the distal small bowel commonly is involved. The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicate colitis. […] Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigella species.

• #1 Food Poisoning: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/175569-overview

  In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting on the central nervous system. The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum. […] A major contributor to seafood contamination with foodborne pathogens appears to be naturally occurring biofilm formation. Vibro and Salmonella species, Aeromonas hydrophila, and Listeria monocytogenes are common seafood bacterial pathogens that form biofilms.

• #1 Toxicity and inhibition mechanism of gallic acid on physiology and fermentation performance of Escherichia coli | Bioresources and Bioprocessing | Full Text

  https://bioresourcesbioprocessing.springeropen.com/articles/10.1186/s40643-022-00564-w

  Gallic acid is a natural phenolic acid that has a stress inhibition effect on Escherichia coli. […] The glucose consumption of E. coli was reduced successively with the increase of gallic acid content in the fermentation medium. […] After 20 h of gallic acid stress, cofactor levels (ATP, NAD+ and NADH) of E. coli 3110 were similarly decreased, indicating a more potent inhibitory effect of gallic acid on E. coli. […] The transcriptional analysis revealed that gallic acid altered the gene expression profiles related to five notable differentially regulated pathways. […] The genes related to the two-component system were up-regulated, while the genes associated with ABC-transporter, energy metabolism, carbon metabolism, and fatty acid biosynthesis were down-regulated. […] As a phenolic compound, gallic acid has a stress inhibition effect on E. coli, which can affect the integrity of the cell membrane and damage the hydrophobic structure after entering the cell, thus affecting the physiological metabolism of the cell.

• #1 Mechanism of poisoning – WikiLectures

  https://www.wikilectures.eu/w/Mechanism_of_poisoning

  Ethanol, detergents, and hydrocarbons change the fluidity of the membranes, which is reflected in the function of the membrane components. Changes in membrane microviscosity change the conformation of membrane channels, receptors and enzymes, and thus disrupt their functions (membrane transport, signaling, membrane potential). Membrane fluidity is a control mechanism for heavy metal absorption. […] The binding of poison to hemoglobin […] Oxidation of hemoglobin to methemoglobin […] Cytochrome oxidase inhibition […] Non-specific interactions, binding to the sulfhydryl group -SH. […] Binding of the poison to the active center of the enzyme. […] Sodium channel, nicotine and muscarinic receptors, psychotropic drugs, addictive substances.

• #1 Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000687

  Ingestion of the lectins present in certain improperly cooked vegetables can result in acute GI tract distress, but the mechanism of toxicity is unknown. […] We therefore tested the novel hypothesis that lectin toxicity is due to an inhibitory effect on plasma membrane repair. […] Lectins potently inhibit plasma membrane repair, and hence are toxic to wounded cells. This represents a novel form of protein-based toxicity, one that, we propose, is the basis of plant lectin food poisoning. […] Plant lectins that are not efficiently degraded by digestive enzymes, and that have an affinity for the surface of gut epithelial cells, such as those present in the Leguminosae family, can be poisonous. […] Epithelial cells lining the GI tract in vivo, unlike cells in vitro, are constantly exposed to mechanical stress and, consequently, frequently suffer plasma membrane disruptions.

• #1 Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000687

  Therefore, could the mechanism of lectin toxicity in vivo be due to an inhibitory effect on the exocytosis-based, constitutive membrane repair, and consequent death of wounded gut epithelial cells? […] We have shown here that binding of cell surface glycoproteins by lectins interferes with the exocytotic events associated with membrane repair (mucus secretion) and that lectins potently block repair. […] Lectins, we hypothesize, are toxic when present in the GI tract based on two, inter-related effects. First, resealing failure occurs within the general population of GI tract cells normally exposed to membrane disrupting levels of mechanical stress, leading to their necrosis. The second lectin-induced effect is exocytotic failure within the subpopulation of GI tract cells that normally secrete mucus, leading to a decrease in protective, lubricating mucus secretion and a consequent increase in the incidence of mechanically-induced membrane disruption events.

• #1 Strychnine Toxicosis in Animals – Toxicology – Merck Veterinary Manual

  https://www.merckvetmanual.com/toxicology/rodenticide-poisoning/strychnine-toxicosis-in-animals

  Strychnine is a pesticide that typically causes toxicosis in companion and production animals by accidental ingestion or malicious poisoning. […] Strychnine is metabolized in the liver by microsomal enzymes. […] Strychnine competitively and reversibly inhibits the inhibitory neurotransmitter glycine at postsynaptic neuronal sites in the spinal cord and medulla. This results in unchecked reflex stimulation of motor neurons affecting all the striated muscles. Because the extensor muscles are relatively more powerful than the flexor muscles, they predominate to produce generalized rigidity and tonic-clonic seizures. Death results from anoxia and exhaustion. […] Strychnine and its metabolites are excreted in the urine. Depending on the quantity ingested and treatment measures taken, most of the toxic dose is eliminated within 2448 hours.

• #1 Mechanisms of Toxicity

  https://www.iloencyclopaedia.org/part-iv-66769/toxicology-57951/mechanisms-of-toxicity

  Pharmacokinetics describes the time relationships for chemical absorption, distribution, metabolism (biochemical alterations in the body) and elimination or excretion from the body. […] Toxicity can be described at different biological levels. […] Mechanisms of toxicity can be straightforward or very complex. […] The primary mechanism of action of organophosphates is the inhibition of acetylcholinesterase (AChE) in the brain and peripheral nervous system. […] The primary treatment is the administration of atropine, which blocks the effects of acetylcholine, and the administration of pralidoxime chloride, which reactivates the inhibited AChE. […] Cancer development is a multi-stage process, and critical genes are key to different types of cancer. […] It is known that certain viruses (such as rubella), bacterial infections and drugs (such as thalidomide and vitamin A) will adversely affect development. […] The intent of this article is to give a perspective on several known mechanisms of toxicity and the need for future study.

• #1 Mechanism of central hypopnoea induced by organic phosphorus poisoning | Scientific Reports

  https://www.nature.com/articles/s41598-020-73003-5

  We hypothesized that organophosphorus cholinesterase inhibitors directly impair preBtC. As the administration of Pox was found to significantly reduce the burst amplitude of preBtC, this is the first electrophysiological proof that Pox impairs preBtC activity. […] PAM and atropine can be administered as antidotes for Pox.

• #1 Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy – PubMed

  https://pubmed.ncbi.nlm.nih.gov/27753502/

  Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15-40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. […] Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.

• #1 Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy – University of Iowa

  https://iro.uiowa.edu/esploro/outputs/9984304682602771

  Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. […] The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. […] Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. […] There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. […] New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.

• #1 Protective mechanism of 1-methylhydantoin against lung injury induced by paraquat poisoning | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0222521

  Paraquat (PQ), one of the most widely used herbicides worldwide, causes severe toxic effects in humans and animals. 1-methylhydantoin (MH) is an active ingredient of Ranae Oviductus, which has broad pharmacological activities, e.g., eliminating reactive oxygen species and inhibiting inflammation. This study investigated the effects of MH on lung injury induced by PQ. […] The main mechanism of PQ poisoning is the massive production of superoxide anions, thus, causing oxidative damage and leading to cell death. […] Although multiple organs are involved, the lung is the main target organ of PQ poisoning. The early manifestation of PQ poisoning is acute lung injury, whereas progressive pulmonary fibrosis, a typical feature of PQ poisoning, develops in a later stage, thus leading to a poor prognosis. At present, toxicological mechanisms of PQ are widely acknowledged to be free radical oxidative damage and mitochondrial damage. Therefore, inhibition of oxidative stress injury is an effective treatment for acute lung injury caused by PQ poisoning.

• #1 Protective mechanism of 1-methylhydantoin against lung injury induced by paraquat poisoning | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0222521

  In conclusion, we found that the metabolic patterns in the MH group and PQ+MH group were significantly different, as mainly reflected in the metabolic pathways of phenylalanine, histidine, threonine, glycine, serine, alanine, glutamic acid and asparagine; bile acid biosynthesis; and nicotinate and nicotinamide metabolism. In addition, MH decreased the levels of MDA and TNF- after the PQ poisoning. Our results indicate that MH attenuates paraquat-induced acute lung injury possibly via antioxidant and anti-inflammatory mechanisms. This study is expected to improve the pharmacological effects of MH and provide new ideas for the management of PQ. However, the mechanism of MH requires further study.

• #1 Molecular mechanism of topoisomerase poisoning by the peptide antibiotic albicidin | Nature Catalysis

  https://www.nature.com/articles/s41929-022-00904-1

  The peptide antibiotic albicidin is a DNA topoisomerase inhibitor with low-nanomolar bactericidal activity towards fluoroquinolone-resistant Gram-negative pathogens. […] Albicidin employs a dual binding mechanism where one end of the molecule obstructs the crucial gyrase dimer interface, while the other intercalates between the fragments of cleaved DNA substrate. Thus, albicidin efficiently locks DNA gyrase, preventing it from religating DNA and completing its catalytic cycle. […] The effectiveness of FQs stems from their so-called gyrase poisoning mechanism which exploits an intrinsic DNA cleavage activity of gyrase by converting it into a toxin rather than simply inhibiting its catalytic action. […] The hybrid polyketidepeptide antibiotic albicidin is produced by the Gram-negative plant pathogen Xanthomonas albilineans which causes devastating leaf scald disease in sugarcane.

• #1 Mechanism of bacterial toxins in deadly attacks

  https://www.mpg.de/19063071/mechanism-of-bacterial-toxins-in-deadly-attacks

  A harmful and often deadly substance made by bacteria, a bacterial toxin manipulates host cell functions and disrupts vital cell processes in a living organism. […] Their findings not only reveal how the deadly cargo of the Tc toxin drives the collapse of the cells cytoskeleton but provide an explanation of the toxins high efficiency. […] After binding of the toxin to receptors on the surface of the host cell, it is endocytosed. Structural changes in the complex trigger the opening of a cocoon which contains a toxic enzyme, which is then secreted in a unique injection mechanism via a channel into the cytoplasm of the host cell. It folds and binds to F-actin. Opening of a gate (K185 E265) facilitates NAD+ entry. The following reaction leads to the transfer of the ADP-ribose group to actin. This modification impairs binding of actin-depolymerizing factors to F-actin which leads to actin clumping and ultimately cell death.

• #1 Mechanism of bacterial toxins in deadly attacks

  https://www.mpg.de/19063071/mechanism-of-bacterial-toxins-in-deadly-attacks

  The mechanism of action of Tc toxins has only recently been uncovered to a greater extent by the work of Stefan Raunsers team in structural biology at the Max Planck Institute in Dortmund. Unraveling the structure of the Tc toxin subunits and their assembly by cryo electron microscopy (cryo-EM) enabled us to understand the key steps of toxin activation and membrane penetration, says Raunser. […] There, it unfolds its deadly effect by disturbing the regulation of the cells cytoskeleton, which consists of a network of polymerized actin (F-actin) filaments involved in many essential cellular processes. […] Until recently, it was only known that TccC3 transfers an ADP-ribose group to actin promoting its aberrant polymerization, which leads to actin filament clumping. […] TccC3 then opens a gate, which brings the molecule NAD+ that contains the ADP-ribose group within striking distance to a reactive site on actin. Once the bulky ADP-ribose group is transferred to F-actin, it is no longer accessible for its depolymerizing factors, whereby F-actin can no longer be broken down and thus clumps. […] When the enzyme detaches from F-actin, its gate mechanism prevents a futile rebinding to the already modified actin as preparation for the next attack. It is amazing how all these mechanisms evolved to increase the toxins potency to the max.

• #2 Poisoning | pathology | Britannica

  https://www.britannica.com/science/poisoning

  Poisoning involves four elements: the poison, the poisoned organism, the injury to the cells, and the symptoms and signs or death. These four elements represent the cause, subject, effect, and consequence of poisoning. To initiate the poisoning, the organism is exposed to the toxic chemical. […] Toxicology is the study of poisons, their action, their detection, and the treatment of conditions they produce.

• #2 Mechanism and Health Effects of Heavy Metal Toxicity in Humans | IntechOpen

  https://www.intechopen.com/chapters/64762

  As such, heavy metal toxicity can have several consequences in the human body. It can affect the central nervous function leading to mental disorder, damage the blood constituents and may damage the lungs, liver, kidneys and other vital organs promoting several disease conditions. […] The various mechanisms that lead to heavy metal toxicity with emphasis on macromolecule and cellular damages, carcinogenesis, neurotoxicity and the molecular basis for their noxious effects. […] The mechanism of free radical generation is specific to the type of heavy metal. […] The main mechanism of heavy metal toxicity include the generation of free radicals to cause oxidative stress, damage of biological molecules such as enzymes, proteins, lipids, and nucleic acids, damage of DNA which is key to carcinogenesis as well as neurotoxicity.

• #2 Mechanism and Health Effects of Heavy Metal Toxicity in Humans | IntechOpen

  https://www.intechopen.com/chapters/64762

  Heavy metal-bound proteins may be a substrate for certain enzymes. In such situations, the heavy metal-bound protein fits into an enzyme in a highly specific pattern to form an enzyme-substrate complex and thus cannot accommodate any other substrate until it is freed. […] Heavy metals may also inhibit protein folding. […] Heavy metal may cause proteins to aggregate as arsenite-induced protein aggregation was observed and shown to be concentration-dependent. […] Heavy metal-induced carcinogenesis includes epigenetic alterations, damage to the dynamic DNA maintenance system and generation of ROS. […] The mechanism of lead-induced carcinogenic process is postulated to induce DNA damage, disrupt DNA repair system and cellular tumor regulatory genes through the generation of ROS. […] The proposed mechanism of mercury-induced cancer is through the generation of free radicals inducing oxidative stress thereby damaging biomolecules.

• #2 Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy – PubMed

  https://pubmed.ncbi.nlm.nih.gov/27753502/

  Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15-40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. […] Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.

• #2 Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5363978/

  CO-mediated reductions in oxygen delivery and mitochondrial oxidative phosphorylation produce ischemic and anoxic brain injury, leading to cognitive deficits in survivors. […] The pathophysiology of CO poisoning involves the reduction of global oxygen delivery and the inhibition of mitochondrial respiration. […] The inflammatory cascade driven by NO and ROS contributes to neurological and cardiac injuries from CO poisoning. […] CO-induced mitochondrial inhibition could cause a stunned myocardium-like syndrome (with hypokinesia in the setting of unobstructed coronary arteries).

• #2 Organophosphate Toxicity: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/167726-overview

  Organophosphate toxicity is a clinical diagnosis. Confirmation of organophosphate poisoning is based on the measurement of cholinesterase activity; but typically, these results are not readily available. […] The primary mechanism of action of organophosphate pesticides is inhibition of carboxyl ester hydrolases, particularly acetylcholinesterase (AChE). AChE is an enzyme that degrades the neurotransmitter acetylcholine (ACh) into choline and acetic acid. […] Organophosphates inactivate AChE by phosphorylating the serine hydroxyl group located at the active site of AChE. Over a period of time, phosphorylation is followed by loss of an organophosphate leaving group and the bond with AChE becomes irreversible, a process known as aging. […] Once AChE has been inactivated, ACh accumulates throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic receptors. Clinical effects are manifested via activation of the autonomic and central nervous systems and at nicotinic receptors on skeletal muscle. […] Organophosphates can be absorbed cutaneously, ingested, inhaled, or injected. Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure, and rate of metabolic degradation.

• #2 Organophosphate poisoning – Wikipedia

  https://en.wikipedia.org/wiki/Organophosphate_poisoning

  Organophosphate poisoning is poisoning due to organophosphates (OPs). Organophosphates are used as insecticides, medications, and nerve agents. […] The underlying mechanism involves the inhibition of acetylcholinesterase (AChE), leading to the buildup of acetylcholine (ACh) in the body. […] The health effects associated with organophosphate poisoning are a result of excess acetylcholine (ACh) present at different nerve synapses and neuromuscular junctions across the body. Specifically, acetylcholinesterase (AChE), the enzyme that normally and constantly breaks down acetylcholine, is inhibited by the organophosphate substance. ACh accumulates in the parasympathetic nervous system, the central nervous system, and in nicotinic neuromuscular junctions. […] Organophosphate inhibition of AChE may be reversible or irreversible, depending on whether covalent bonding (also called „aging” in this context) occurs. […] Chemically, organophosphates cause poisoning by phosphorylating the serine hydroxyl residue on AChE, which inactivates AChE. This causes disturbances across the cholinergic synapses and can only be reactivated very slowly, if at all.

• #2 Cyanide poisoning – Wikipedia

  https://en.wikipedia.org/wiki/Cyanide_poisoning

  Cyanide is a potent cytochrome c oxidase (COX, a.k.a. Complex IV) inhibitor, causing asphyxiation of cells. As such, cyanide poisoning is a form of histotoxic hypoxia, because it interferes with the ability of cells to take or use oxygen via oxidative phosphorylation. […] Specifically, cyanide binds to the heme a3-CuB binuclear center of COX (and thus is a non-competitive inhibitor of it). This prevents electrons passing through COX from being transferred to O2, which not only blocks the mitochondrial electron transport chain, it also interferes with the pumping of a proton out of the mitochondrial matrix which would otherwise occur at this stage. Therefore, cyanide interferes not only with aerobic respiration but also with the ATP synthesis pathway it facilitates, owing to the close relationship between those two processes.

• #2 Poisoning – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/poisoning/

  Cyanide blocks the electron transport chain by binding to cytochrome complex IV oxidative phosphorylation anaerobic metabolism, lactic acid, histotoxic hypoxia. […] Cyanide poisoning is primarily a clinical diagnosis. […] Cyanide poisoning is primarily a clinical diagnosis. […] Do not delay empiric antidotal treatment if cyanide poisoning is suspected. […] Hydroxocobalamin is the first-line antidote for cyanide poisoning. […] Nitrites induce methemoglobinemia by oxidizing hemoglobin to create methemoglobin. […] Sodium thiosulfate supplies sulfur donors to the mitochondrial enzyme rhodanese.

• #2

  https://link.springer.com/article/10.1007/s13181-019-00710-5

  Hydrogen sulfide (H2S) is found in various settings. […] In this paper we performed a review of the available literature on the mechanism of toxicity, clinical presentation, and development of countermeasures for H2S toxicity. […] In vivo, H2S undergoes an incomplete oxidation after an exposure. The remaining non-oxidized H2S is found in dissolved and combined forms. […] The combined non-soluble forms are found as acid-labile sulfides and sulfhydrated proteins, which play a role in toxicity. […] Recent countermeasure development takes into account the toxicokinetics of H2S. […] Some countermeasures focus on binding free hydrogen sulfide (hydroxocobalamin, cobinamide); some have direct effects on the mitochondria (methylene blue), while others work by mitigating end organ damage by generating other substances such as nitric oxide (NaNO2).

• #2 Mechanism and Health Effects of Heavy Metal Toxicity in Humans | IntechOpen

  https://www.intechopen.com/chapters/64762

  Nickel has an extensive range of carcinogenic mechanisms which include regulation of transcription factors, controlled expression of certain genes and generation of free radicals. […] Some heavy metals such as lead and manganese may affect the brain and cause neurological toxicity. […] Lead can impair learning and memory in the brain by inhibiting the N-methyl-d-aspartate receptor (NMDAR) and can block neurotransmission by inhibit neurotransmitter release, block the neuronal voltage-gated calcium (Ca2+) channels (VGCCs) and reduce the expression of brain-derived neurotrophic factor (BDNF). […] Manganese is known to accumulate in the mitochondria of neurons, astrocytes and oligodendrocytes cells and disrupts ATP synthesis by inhibiting the F1/F0 ATP synthase or complex 1 (NADH dehydrogenase) of the mitochondrial respiration chain. […] The disruption of ATP synthesis by manganese leads to decreased intracellular ATP levels and generation of free radicals thereby increasing oxidative stress which may contribute to manganese cellular toxicity.

• #2 Food Poisoning: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/175569-overview

  Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The pathogenesis of diarrhea in food poisoning is classified broadly into either noninflammatory or inflammatory types. Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory mechanisms of the mucosa of the small intestine, without invasion. This leads to large volume watery stools in the absence of blood, pus, or severe abdominal pain. Occasionally, profound dehydration may result. The enterotoxins may be either preformed before ingestion or produced in the gut after ingestion. Examples include Vibrio cholerae, enterotoxic Escherichia coli, Clostridium perfringens, Bacillus cereus, Staphylococcus organisms, Giardia lamblia, Cryptosporidium, rotavirus, norovirus, and adenovirus.

• #2 Food Poisoning: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/175569-overview

  Inflammatory diarrhea is caused by the action of cytotoxins on the mucosa, leading to invasion and destruction. The colon or the distal small bowel commonly is involved. The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicate colitis. […] Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigella species.

• #2 Food Poisoning: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/175569-overview

  In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting on the central nervous system. The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum. […] A major contributor to seafood contamination with foodborne pathogens appears to be naturally occurring biofilm formation. Vibro and Salmonella species, Aeromonas hydrophila, and Listeria monocytogenes are common seafood bacterial pathogens that form biofilms.

• #2 Toxicity and inhibition mechanism of gallic acid on physiology and fermentation performance of Escherichia coli | Bioresources and Bioprocessing | Full Text

  https://bioresourcesbioprocessing.springeropen.com/articles/10.1186/s40643-022-00564-w

  Gallic acid is a natural phenolic acid that has a stress inhibition effect on Escherichia coli. […] The glucose consumption of E. coli was reduced successively with the increase of gallic acid content in the fermentation medium. […] After 20 h of gallic acid stress, cofactor levels (ATP, NAD+ and NADH) of E. coli 3110 were similarly decreased, indicating a more potent inhibitory effect of gallic acid on E. coli. […] The transcriptional analysis revealed that gallic acid altered the gene expression profiles related to five notable differentially regulated pathways. […] The genes related to the two-component system were up-regulated, while the genes associated with ABC-transporter, energy metabolism, carbon metabolism, and fatty acid biosynthesis were down-regulated. […] As a phenolic compound, gallic acid has a stress inhibition effect on E. coli, which can affect the integrity of the cell membrane and damage the hydrophobic structure after entering the cell, thus affecting the physiological metabolism of the cell.

• #2 Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000687

  Therefore, could the mechanism of lectin toxicity in vivo be due to an inhibitory effect on the exocytosis-based, constitutive membrane repair, and consequent death of wounded gut epithelial cells? […] We have shown here that binding of cell surface glycoproteins by lectins interferes with the exocytotic events associated with membrane repair (mucus secretion) and that lectins potently block repair. […] Lectins, we hypothesize, are toxic when present in the GI tract based on two, inter-related effects. First, resealing failure occurs within the general population of GI tract cells normally exposed to membrane disrupting levels of mechanical stress, leading to their necrosis. The second lectin-induced effect is exocytotic failure within the subpopulation of GI tract cells that normally secrete mucus, leading to a decrease in protective, lubricating mucus secretion and a consequent increase in the incidence of mechanically-induced membrane disruption events.

• #2 Protective mechanism of 1-methylhydantoin against lung injury induced by paraquat poisoning | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0222521

  Paraquat (PQ), one of the most widely used herbicides worldwide, causes severe toxic effects in humans and animals. 1-methylhydantoin (MH) is an active ingredient of Ranae Oviductus, which has broad pharmacological activities, e.g., eliminating reactive oxygen species and inhibiting inflammation. This study investigated the effects of MH on lung injury induced by PQ. […] The main mechanism of PQ poisoning is the massive production of superoxide anions, thus, causing oxidative damage and leading to cell death. […] Although multiple organs are involved, the lung is the main target organ of PQ poisoning. The early manifestation of PQ poisoning is acute lung injury, whereas progressive pulmonary fibrosis, a typical feature of PQ poisoning, develops in a later stage, thus leading to a poor prognosis. At present, toxicological mechanisms of PQ are widely acknowledged to be free radical oxidative damage and mitochondrial damage. Therefore, inhibition of oxidative stress injury is an effective treatment for acute lung injury caused by PQ poisoning.

• #2 Mechanism of bacterial toxins in deadly attacks

  https://www.mpg.de/19063071/mechanism-of-bacterial-toxins-in-deadly-attacks

  The mechanism of action of Tc toxins has only recently been uncovered to a greater extent by the work of Stefan Raunsers team in structural biology at the Max Planck Institute in Dortmund. Unraveling the structure of the Tc toxin subunits and their assembly by cryo electron microscopy (cryo-EM) enabled us to understand the key steps of toxin activation and membrane penetration, says Raunser. […] There, it unfolds its deadly effect by disturbing the regulation of the cells cytoskeleton, which consists of a network of polymerized actin (F-actin) filaments involved in many essential cellular processes. […] Until recently, it was only known that TccC3 transfers an ADP-ribose group to actin promoting its aberrant polymerization, which leads to actin filament clumping. […] TccC3 then opens a gate, which brings the molecule NAD+ that contains the ADP-ribose group within striking distance to a reactive site on actin. Once the bulky ADP-ribose group is transferred to F-actin, it is no longer accessible for its depolymerizing factors, whereby F-actin can no longer be broken down and thus clumps. […] When the enzyme detaches from F-actin, its gate mechanism prevents a futile rebinding to the already modified actin as preparation for the next attack. It is amazing how all these mechanisms evolved to increase the toxins potency to the max.

• #3 Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5363978/

  Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. […] The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. […] CO binds to hemoglobin (Hb) in the blood with high affinity, forming COHb. […] CO binding to Hb also stabilizes the relaxed, high-affinity quaternary state of Hb (known as R-state), increasing the affinity for oxygen of other sites within the Hb tetramer, and further reducing oxygen release and delivery. […] CO inhibits mitochondrial respiration by binding the ferrous heme a3 in the active site of COX, effectively shutting down oxidative phosphorylation, similar to the effects of cyanide and nitric oxide (NO).

• #3 Organophosphate Toxicity: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/167726-overview

  Organophosphate toxicity is a clinical diagnosis. Confirmation of organophosphate poisoning is based on the measurement of cholinesterase activity; but typically, these results are not readily available. […] The primary mechanism of action of organophosphate pesticides is inhibition of carboxyl ester hydrolases, particularly acetylcholinesterase (AChE). AChE is an enzyme that degrades the neurotransmitter acetylcholine (ACh) into choline and acetic acid. […] Organophosphates inactivate AChE by phosphorylating the serine hydroxyl group located at the active site of AChE. Over a period of time, phosphorylation is followed by loss of an organophosphate leaving group and the bond with AChE becomes irreversible, a process known as aging. […] Once AChE has been inactivated, ACh accumulates throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic receptors. Clinical effects are manifested via activation of the autonomic and central nervous systems and at nicotinic receptors on skeletal muscle. […] Organophosphates can be absorbed cutaneously, ingested, inhaled, or injected. Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure, and rate of metabolic degradation.

• #3 Poisoning – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/poisoning/

  Cyanide blocks the electron transport chain by binding to cytochrome complex IV oxidative phosphorylation anaerobic metabolism, lactic acid, histotoxic hypoxia. […] Cyanide poisoning is primarily a clinical diagnosis. […] Cyanide poisoning is primarily a clinical diagnosis. […] Do not delay empiric antidotal treatment if cyanide poisoning is suspected. […] Hydroxocobalamin is the first-line antidote for cyanide poisoning. […] Nitrites induce methemoglobinemia by oxidizing hemoglobin to create methemoglobin. […] Sodium thiosulfate supplies sulfur donors to the mitochondrial enzyme rhodanese.

• #3 Toxicity and inhibition mechanism of gallic acid on physiology and fermentation performance of Escherichia coli | Bioresources and Bioprocessing | Full Text

  https://bioresourcesbioprocessing.springeropen.com/articles/10.1186/s40643-022-00564-w

  Gallic acid is a natural phenolic acid that has a stress inhibition effect on Escherichia coli. […] The glucose consumption of E. coli was reduced successively with the increase of gallic acid content in the fermentation medium. […] After 20 h of gallic acid stress, cofactor levels (ATP, NAD+ and NADH) of E. coli 3110 were similarly decreased, indicating a more potent inhibitory effect of gallic acid on E. coli. […] The transcriptional analysis revealed that gallic acid altered the gene expression profiles related to five notable differentially regulated pathways. […] The genes related to the two-component system were up-regulated, while the genes associated with ABC-transporter, energy metabolism, carbon metabolism, and fatty acid biosynthesis were down-regulated. […] As a phenolic compound, gallic acid has a stress inhibition effect on E. coli, which can affect the integrity of the cell membrane and damage the hydrophobic structure after entering the cell, thus affecting the physiological metabolism of the cell.

• #4 Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5363978/

  Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. […] The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. […] CO binds to hemoglobin (Hb) in the blood with high affinity, forming COHb. […] CO binding to Hb also stabilizes the relaxed, high-affinity quaternary state of Hb (known as R-state), increasing the affinity for oxygen of other sites within the Hb tetramer, and further reducing oxygen release and delivery. […] CO inhibits mitochondrial respiration by binding the ferrous heme a3 in the active site of COX, effectively shutting down oxidative phosphorylation, similar to the effects of cyanide and nitric oxide (NO).

• #4 Poisoning – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/poisoning/

  Cyanide blocks the electron transport chain by binding to cytochrome complex IV oxidative phosphorylation anaerobic metabolism, lactic acid, histotoxic hypoxia. […] Cyanide poisoning is primarily a clinical diagnosis. […] Cyanide poisoning is primarily a clinical diagnosis. […] Do not delay empiric antidotal treatment if cyanide poisoning is suspected. […] Hydroxocobalamin is the first-line antidote for cyanide poisoning. […] Nitrites induce methemoglobinemia by oxidizing hemoglobin to create methemoglobin. […] Sodium thiosulfate supplies sulfur donors to the mitochondrial enzyme rhodanese.

• #5 Poisoning – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/poisoning/

  Cyanide blocks the electron transport chain by binding to cytochrome complex IV oxidative phosphorylation anaerobic metabolism, lactic acid, histotoxic hypoxia. […] Cyanide poisoning is primarily a clinical diagnosis. […] Cyanide poisoning is primarily a clinical diagnosis. […] Do not delay empiric antidotal treatment if cyanide poisoning is suspected. […] Hydroxocobalamin is the first-line antidote for cyanide poisoning. […] Nitrites induce methemoglobinemia by oxidizing hemoglobin to create methemoglobin. […] Sodium thiosulfate supplies sulfur donors to the mitochondrial enzyme rhodanese.

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