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pubmed:abstractText |
Aluminium and zinc phosphides are highly effective insecticides and rodenticides and are used widely to protect grain in stores and during its transportation. Acute poisoning with these compounds may be direct due to ingestion of the salts or indirect from accidental inhalation of phosphine generated during their approved use. MECHANISMS OF TOXICITY: Both forms of poisoning are mediated by phosphine which has been thought to be toxic because it inhibits cytochrome c oxidase. While phosphine does inhibit cytochrome C oxidase in vitro, the inhibition is much less in vivo. It has been shown recently in nematodes that phosphine rapidly perturbs mitochondrial morphology, inhibits oxidative respiration by 70%, and causes a severe drop in mitochondrial membrane potential. This failure of cellular respiration is likely to be due to a mechanism other than inhibition of cytochrome C oxidase. In addition, phosphine and hydrogen peroxide can interact to form the highly reactive hydroxyl radical and phosphine also inhibits catalase and peroxidase; both mechanisms result in hydroxyl radical associated damage such as lipid peroxidation. The major lethal consequence of phosphide ingestion, profound circulatory collapse, is secondary to factors including direct effects on cardiac myocytes, fluid loss, and adrenal gland damage. In addition, phosphine and phosphides have corrosive actions.
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