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(A) the cause of poisoning
Organic and inorganic cyanide is widely used in industrial and agricultural production, particularly common cyanide electroplating industry, it is easy to obtain, are often used to commit suicide or homicide. People often consume large amounts of improper handling or untreated almond, cassava Erzhi accidental poisoning.
(B) the toxicological effect
Cyanide into the body break down toxic cyanide ion issued (CN-), cyanide ions within the tissue cells can inhibit the activity of 42 enzymes such as cytochrome oxidase, peroxidase, decarboxylase, succinic dehydrogenase and lactate dehydrogenase. Which cytochrome oxidase is most sensitive to cyanide. Cyanide ion can rapidly and oxidized cytochrome oxidase in the combination of ferric iron to prevent its reduction into ferrous iron, so that transmission electron oxidation process is interrupted, cells can not use the oxygen in the blood caused by suffocation. Central nervous system most sensitive to hypoxia, it is first of all the brain damage, leading to central respiratory failure and death. In addition, the release of cyanide in the digestive tract has a corrosive effect of hydroxide ions. Inhalation of high concentrations of cyanide, hydrogen cyanide, or swallow a lot of those in respiratory arrest within 2-3 minutes, was "electric shock-like" death.
(C) the amount of toxic and lethal dose
Oral lethal dose of hydrocyanic acid 0.7 ~ 3.5mg/kg; inhalation of hydrogen cyanide concentration of the air in the 0.5mg / L can be lethal; oral administration of sodium cyanide, potassium cyanide, a lethal dose of 1 ~ 2mg/kg. Adults take one bitter almond 40 60, 10 to 20 children with poisoning and even death can occur. Untreated cassava lethal dose 150 ~ 300g. In addition many cyanide compounds (eg potassium cyanide, sodium cyanide and electroplating, photographic dyes often containing cyanide used in drugs) can cause acute poisoning.
(D) Clinical manifestations
High-dose poisoning often occurs with lightning speed coma and death. A few seconds after the intake screamed, cyanosis, convulsions, respiratory arrest immediately. Low-dose poisoning can occur 15 to 40 minutes of poisoning process: numbness of mouth and throat, salivation, headache, nausea, chest tightness, breathing speed up the deeper, the pulse speed up, arrhythmias, miosis, bright red skin and mucous membranes, convulsions, coma Finally, loss of consciousness and death.
General clinical manifestations of acute poisoning can be divided into four phases:
(1) prodromal phase: oral poisoning with mouth, throat, burning sensation, nausea and vomiting, vomit, bitter almond flavor, accompanied by headache, dizziness, fatigue, tinnitus, chest tightness, stool urgency and so on. Inhalation poisoning may have eyes, throat and upper respiratory tract irritation. After narrowing the pupil to expand on both sides of the first, then quickly blurred consciousness, coma.
(2) of difficulty breathing: diff
(3) seizure phase: tonic or paroxysmal convulsions, and even opisthotonus, incontinence, loss of consciousness.
(4) paralysis of: muscle relaxation, reflex, slow shallow breathing, and finally breathing, cardiac arrest.
(E) Autopsy findings
Cyanide in the blood of heme formation, so Shiban, muscle and blood showed a bright red. Those who died quickly, the body organs obvious signs of suffocation. Oral poisoning, digestive tract are visible edema, stomach and duodenal mucosa congestion, erosion, necrosis, stomach and body cavity bitter almond flavor. Inhalation of cyanide poisoning death, brain, hippocampus, striatum, substantia nigra edema, nerve cell degeneration and necrosis, gliosis, heart, liver, cloudy swelling of renal parenchymal cells.
Medical HEALTH "> Preventive Medicine>> Toxicology>> Summary of the biochemical mechanism of cyanide intoxication comments recommended online download full collection of this Wang Mingjun OF COLLEGES Department of Chemistry, Duyun 558000" OF COLLEGES OF "2008 28 No. 3 fast-food prizes Report Summary: From the structure of cyanide, cytochrome oxidase in the respiratory chain structure and a typical bio-oxidation mechanism of cyanide intoxication. The mechanism proposed is the CN-poisoning and the combination of cytochrome oxidase, the structural change of the enzyme can no longer obtain from the electronic substrate, interrupt the biological oxidation process, the cell uptake of a serious shortage of energy, resulting in the lack of human and animal energy death. Number of pages: 3 page range :75-77 Key words: cyanide poisoning in the structure of cytochrome oxidase mechanism subject classification: R995 [medicine, HEALTH "Medicine> Toxicology (Toxicology)> inorganic poisons] TQ086.5 [ INDUSTRY AND TECHNOLOGY "Chemical INDUSTRY" general issues> Chemical Plant> Production Safety TECHNOLOGY "dangerous chemical compounds and chemical] Related Articles: Topics related citations (1)
First, the poisoning mechanism
Cyanide ions on the respiratory chain of mitochondria cytochrome oxidase (EC18.104.22.168) with high affinity, and cytochrome oxidase so that the loss of binding activity, thereby blocking cell respiration and oxidative phosphorylation.
Cytochrome oxidase is supplemented based porphyrin protein, contains two heme A groups and two copper atoms, respectively, of cytochrome a and a3. a and a3 has failed to separate the two components, it is cytochrome a and a3 will be collectively known as cytochrome oxidase. Hydrocyanic acid on the inhibition of cytochrome oxidase, mainly CN-and cytochrome a3 in the iron (Fe3) caused by ligand binding.
Oxidized cytochrome oxidase with CN-binding capacity after loss of electron transfer. And even oxygen can not be used, blocked oxidative phosphorylation, ATP synthesis decreased cellular uptake of energy a serious shortage of suffocation.
In vitro experiments show that, KCN1.5 Ã— 10-6M inhibited liver cytochrome oxidase activity of 50%; concentration of 4.2 Ã— 10-2M, the enzyme activity was completely inhibited.
Animal experiments show, poisoning symptoms and activity of cytochrome oxidase inhibition is equal, the enzyme activity is restored, the symptoms disappear. Cyanide inhibition of cytochrome oxidase on the speed and toxic dose and animal categories. Figure 14-3, mice were injected intraperitoneally KCN3mg/kg and 5mg/kg 5 to 15 minutes after the inhibition reached a maximum 70%, recovery time is 20 to 30 minutes.
Cyanide ion can inhibit other enzymes with high heme iron, such as catalase and peroxidase cytochrome C peroxidase complex formation, but the concentration of inhibition of cytochrome oxidase than 1 ~ 2 to orders of magnitude. Some non-heme enzyme metal element, such as tyrosinase, ascorbic acid oxidase, xanthine oxidase, amino acid oxidase, can also form complexes with cyanide ions. But its high concentration of 10-2 ~ 10-3M to present different degrees of inhibition only. In addition, the cyanide containing Schiff base intermediate with the ribose -2- enzyme carboxyl phosphate and 2 - keto -4- hydroxy-glutaric acid salt to form cyanate aldolase inhibit the activity of intermediates.
Second, the toxicological effects
(A) of the central nervous system
Central nervous system on the cyanide ion sensitive, acute cyanide poisoning can cause certain brain regions and spinal cord degeneration of phosphate ester. At the same time in a variety of cyanide inhibition of enzyme systems, metabolic changes in the medium, Ca concentration significantly increased and membrane peroxidation ester enhanced antioxidant defense system damage, oxidative phosphorylation can not use the blocks and tissue of oxygen and so on. The changes in the toxicity of oxygen present. First, the central function of the cortex affected. Small dose of hydrogen cyanide can cause cortical inhibition, conditioned reflex disappeared. Severe poisoning, central nervous system inhibition showed from top to bottom. Changes in brain electrical activity consistent with the central activities, such as a monkey, cat, intravenous injection of NaCN, the first motor cortex regional activities reduced or lost, followed by the nucleus of the hypothalamus, midbrain, reticular formation and extension of brain electrical activity have been suppressed. EEG activity is restored, then start with the lower part of the start, bottom-up retrograde recovery.
(B) of the respiratory system
Small doses cause respiratory excited; large doses, respiratory inhibition after the first excitement. First accelerated in the deep breathing, then apnea, irregular breathing, and then again a second respiratory arrest. Paralysis of the respiratory center is the main reason for hydrogen cyanide poisoning. Changes in respiratory function caused by cyanide factors: â‘ the direct effect on the respiratory center; â‘¡ excited carotid body and aortic body chemoreceptor reflex respiratory center excitability. Cut off the neural pathway excitability was significantly reduced breathing; â‘¢ hypoxia, energy metabolism disorders, changes in blood pH; â‘£ respiratory muscle spasm and paralysis.
(C) of the circulatory system
Small dose of cyanide on the cardiovascular excitatory effects, the performance of heart rate, cardiac output increases, blood pressure, then gradually returned to normal. If the toxic dose larger, after following the excitement, there may be suppression, bradycardia, decreased cardiac output, blood pressure, until the heart stops. Heart rate can be maintained in a few minutes after breathing stops. Circulatory failure also contributed to the cyanide poisoning death of one of the reasons. The factors causing these changes are: â‘ the cyanide ion on cardiovascular exercise and the direct effect of the central; â‘¡ aortic body and carotid body chemoreceptor reflex function; â‘¢ direct effect on the heart. Experiments show that injection of small doses of human intravenous NaCN (0.11 ~ 0.2mg/kg), ECG sinus arrest, sinus arrhythmia, heart rate to gradually speed up, 3 minutes back to normal. Lethal dose of inhaled hydrogen cyanide, there slow heart rate, sinus arrhythmia, P wave disappeared, atrioventricular block, ventricular fibrillation; QRS wave voltage and morphological changes may have, T wave amplitude increases, ST segment shortening and even disappear. ECG after poisoning is a complex mechanism, the early changes may be neurogenic, is the central toxic effects of reflection or result of the change late cyanide ions on the heart may be the direct damage and hypoxia. â‘£ direct expansion of peripheral vascular function and tissue toxicity of oxygen and so on.
(D) changes in metabolism
Cyanide toxicity caused by tissue hypoxia and cellular metabolism changes include: aerobic oxidative metabolism blocked, anaerobic metabolism increased, decreased oxidative phosphorylation, ATP / ADP ratio of reduced or even reversed; glucose, lactate and ino
Experiments show that rats injected KCN spasm, the Î³-aminobutyric acid in brain tissue significantly reduced glutaredoxin acid content increased significantly, the concentration of intracellular Ca2 increase and neurotransmitter release; blood oxidized glutathione levels decreased rapidly , has increased the total glutathione; the â…¦ prothrombin and coagulation factor deficiency, reducing the blood coagulation; thiocyanate in blood and urine were significantly increased. Temperature drops with the toxic dose, the dose the greater the reduction was even worse.