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Hydrogen sulfide is a chemical compound with the formula H 2 S.It is a colorless chalcogen-hydride gas, and is poisonous, corrosive, and flammable, with trace amounts in ambient atmosphere having a characteristic foul odor of rotten eggs. [11]
In 1832, a certain John Bodle was brought to trial for poisoning his grandfather by putting arsenic in his coffee. James Marsh, a chemist working at the Royal Arsenal in Woolwich, was called by the prosecution to try to detect its presence. He performed the standard test by passing hydrogen sulfide through the suspect fluid.
An example of histotoxic hypoxia is cyanide poisoning. There is a profound drop in tissue oxygen consumption since the reaction of oxygen with cytochrome oxidase is blocked by the presence of cyanide. Cyanide binds to the ferric ion on cytochrome oxidase a 3 and prevents the fourth and final reaction in the electron transport chain.
While the determination of the specific toxin can be time-consuming due to the number of different substances that can cause injury or death, certain clues can narrow down the possibilities. For example, carbon monoxide poisoning would result in bright red blood while death from hydrogen sulfide poisoning would cause the brain to have a green hue.
Treatment of sulfur with hydrogen gives hydrogen sulfide.When dissolved in water, hydrogen sulfide is mildly acidic: [5] H 2 S ⇌ HS − + H +. Hydrogen sulfide gas and the hydrosulfide anion are extremely toxic to mammals, due to their inhibition of the oxygen-carrying capacity of hemoglobin and certain cytochromes in a manner analogous to cyanide and azide.
To reduce the extra sulfur in the ruminant's diet, ruminal bacteria break the excess down, resulting in Hydrogen Sulfide, which is soluble in water, but as temperature increases, the solubility decreases, which leads to the hydrogen sulfide gas being reinhaled by the animal, causing sulfur induced polioencephalomalacia.
Poisoning often involves compounds that chemically bond to a catalyst's active sites. Poisoning decreases the number of active sites, and the average distance that a reactant molecule must diffuse through the pore structure before undergoing reaction increases as a result. [4] As a result, poisoned sites can no longer alter the rate of reaction ...
Sulfur medications such as phenacetin, metoclopramide, dapsone, phenzopyridine, and trimethoprim-sulfamethoxazole; hydrogen-sulfide-producing intestinal bacteria, such as Morganella morganii: Risk factors: Pulmonary arteriovenous malformation: Prevention: Avoidance of sulfur-containing compounds including drugs: Treatment: Blood transfusions