Aluminum Phosphide Poisoning in Animals

Abstract

Several articles have showed the effect of ALP toxicity on different organs. Toxicity mechanisms are not clearly understood yet. Due to the potential increased use of ALP as a fumigant and the lack of adequate toxicity data, previous studies were re-evaluated to characterize the epidemiological, toxicological, and clinical/ pathological aspects of ALP poisoning and its management. Related terms were looked up in bibliographical databases such as the Tehran University Medical Science Digital Library, PubMed, Scopus, Google Scholar, and British library. The studies suggest that phosphine targets the mitochondria and inhibits respiration in rat liver mitochondria, insect mitochondria, and intact nematodes. On the other hand, glutathione (GSH) levels are reduced in various tissues of ALP-poisoned rats, while remaining unchanged in insects and mammalian cells. Also, acetylcholine signaling is an important component of phosphine toxicity. Phosphine (PH3) induces oxidative stress and lipid peroxidation in insects, mammalian cells, and other animals. There is no known antidote for ALP intoxication; but, melatonin as an effective antidote protects against oxidative damage in the brain, lung, and liver of the rats and suggests the involvement of ROS in the genotoxicity of PH3. Cholinesterase inhibition responds to treatment with atropine, pralidoxime, and oral sweet almond oil, especially if used immediately after ALP poisoning. Several treatments have been used in animals some of which have not been tested in human-beings yet. Such treatments should be given in controlled situations with the hope they may be helpful in treating these patients.