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.