The cardioprotective effects of cerium oxide nanoparticles against the poisoning generated by aluminum phosphide pesticide: Controlling oxidative stress and mitochondrial damage

Background: Aluminum phosphide (AlP) is a well-known toxic compound used as an agricultural pesticide to prevent insect damage to stored crops. However, even if just a small amount was consumed, it caused lasting harm to the human body and, in acute concentrations, death. The current study employed cerium oxide nanoparticles (CeO₂ NPs) to reduce oxidative stress and various harmful outcomes of AlP poisoning. Methods: Following finding effective concentrations of CeO₂ NPs via MTT assay, Human Cardiac Myocyte (HCM) cells were pre-treated with CeO₂ NPs for 24 h. After that, they were exposed to 2.36 μM AlP. The activity of oxidative stress and mitochondrial biomarkers, including mitochondrial swelling, mitochondrial membrane potential, and cytochrome c release, were evaluated in HCM cells. Finally, the population of apoptotic and necrotic cells was assessed via flow cytometry. Results: After 24 h, data revealed that all tested concentrations of CeO₂ NPs were safe, and 25 and 50 μM of that were selected as effective concentrations. Oxidative stress markers (malondialdehyde, protein carbonyl, superoxide dismutase, and catalase) showed that CeO₂ NPs could successfully decrease AlP poisoning due to their antioxidant characteristics. Mitochondrial markers were also recovered by pre-treatment of HCM cells with CeO₂ NPs. Furthermore, pre-treating with CeO₂ NPs could compensate for the reduction of live cells with AlP and cause a diminishing in the population of early and late apoptotic cells. Conclusion: As a result, it is evident that CeO₂ NPs, through the recovery of oxidative stress and mitochondrial damages caused by AlP, reduce apoptosis and have therapeutic potentials on HCM cells.