Arsenic reversibly binds with sulfhydryl groups found in many tissues and enzyme systems. The mechanisms of toxicity for inorganic arsenic are as follows:
1. For arsenite, inhibition of the pyruvate dehydrogenase complex is the primary biochemical lesion. This inhibition results in diminished adenosine triphosphate (ATP) production and, indirectly, in decreased gluconeogenesis, possibly leading to hypoglycemia. Arsenic also interferes with insulin-dependent cellular glucose uptake.14
2. For arsenate, uncoupling of oxidative phosphorylation and loss of ATP occur when As5+ substitutes for inorganic phosphate in one step of the glycolysis reaction.
Pathologically, acute exposure produces dilation and increased permeability of small blood vessels, resulting in gastrointestinal mucosal and submucosal inflammation and necrosis, cerebral edema and hemorrhage, myocardial tissue destruction, and fatty degeneration of the liver and kidneys. Subacute or chronic exposure can cause a primary peripheral axonal neuropathy with secondary demyelination.
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