Protective role of coenzyme Q10 as a means of alleviating the toxicity of aluminum phosphide: An evidence-based review.

Aluminum phosphide, which is known as rice tablet in Iran, is being used in an increasing number of cases of self-poisoning, and such cases have a high mortality rate. This poisoning has become an important problem in various developing countries. There is no specific antidote, and supportive care usually fails to restore cardiac systolic function and to resolve the patient's severe hypotension. The main mechanism of action of aluminum phosphide is believed to be an inhibition of cytochrome c oxidase in mitochondria followed by a stoppage of cellular metabolism. Currently, scientific attention is exploring modifying the functioning of mitochondria using various novel therapeutic agents. One such agent is coenzyme Q10, which has an important role in the mitochondrial electron transport chain. It is hydrophobic in nature acting as an antioxidant with the ability to scavenge oxygen-derived free radicals. As a result of these properties, coenzyme Q10 has a crucial role to play in reducing cellular oxidative stress. Moreover, there is evidence suggesting that coenzyme Q10 is able to enhance cardiac systolic function in heart failure patients. Based on the above, we propose that treating patients suffering from aluminum phosphide poisoning with coenzyme Q10 may be able to mitigate mitochondrial dysfunction and improve heart contractility. This novel therapeutic intervention enables this by removing oxygen-derived free radicals from the mitochondria and modifying mitochondrial functioning. We believe that this treatment has potential as an effective adjunct to supportive care in cases of aluminum phosphide poisoning and should also help to alleviate tissue injury. [ABSTRACT FROM AUTHOR]