Induced cytotoxicity caused the mitochondrial damages and oxidative stress by Aluminum phosphide; an overview of the mechanism to the clinic

Aluminum phosphide (AlP) is a significant fumigant and a notable, highly effective pesticide for both indoor and outdoor use. Analytical tests like the gas chromatographic method in post-mortem specimens and survivors have been developed to assess the quantity of phosphine and to differentiate between ZnP and AlP poisoning, even if clinical history can usually aid in making the final diagnosis. In this way, it is demonstrated that mitochondrial failure caused ALP to create reactive oxygen species (ROS). As a result of red blood cell hemolysis, decreased ATP synthesis, and the activation of apoptosis in cardiomyocytes brought on by ROS generation, different problems eventually develop. Since cardiomyocytes are the cells that are most significantly affected by ALP, using the right therapeutic methods to get the cells working again will prolong patient survival. Correspondingly, Phosphine's ability to inhibit cytochrome c oxidase has been demonstrated in vitro. It seems improbable that this interaction is the main driver of its toxicity, though. ALP poisoning may cause the most damage to the mitochondria, which might lead to poor ATP synthesis, metabolic shutdown, and multiorgan dysfunction (MOD). Additionally, due to an impairment in electron flow, there may be free radical formation and damage, which could also result in MOD. Rats and insects have shown signs of ALP-induced toxicity brought on by reactive oxygen species. A similar mechanism might potentially be present in people and help fill in the gap in the pathophysiology of ALP poisoning. Cellular poisoning, oxidative stress, cholinesterase inhibition, circulatory failure, cardiotoxicity, gastrointestinal and pulmonary toxicity, hepatic damage, neurological toxicity, electrolyte imbalance, and general metabolic disturbances are just a few of the many effects caused by metal phosphides. In this review article, we discuss the association of cytotoxicity, mitochondrial damage, and oxidative stress by Aluminum phosphide.