The present work was designed to examine the effect of a new (25)Mg(2+)-carrying nanoparticle (PMC16) on energy and oxidative stress parameters inside the heart of the rats exposed to acute mild toxic dose of
malathion, a widely used
organophosphate. Post a single intraperitoneal (ip) injection of
malathion (0.25 of LD50), PMC16 at different doses (0.05, 0.1, and 0.2 of LD50) was administered intravenously (iv) as a supplement to standard
therapy of
atropine and
pralidoxime. MgSO(4) was used as another supplement for comparison with PMC16. Oxidative stress
biomarkers including lipid peroxidation (LPO) and
reactive oxygen species (ROS),
antioxidant enzymes including
superoxide dismutase (SOD),
glutathione peroxidase (GPx),
catalase (CAT),
ATP/
ADP ratio, and Mg in the cardiac cells were determined. Results indicated a significant increase in LPO, ROS,
ADP/
ATP ratio, and a decrease in Mg post-
malathion poisoning in comparison to controls. All of these parameters were improved by use of standard
therapy either with MgSO4 or various doses of PMC16. The activities of SOD, CAT, and GPx did not change significantly in the present acute
malathion poisoning model and neither MgSO(4) or PMC16 had no considerable improvement on these parameters. Comparing groups that received normal Mg and those of various doses of PMC16, a significant difference was found with the PMC16 (0.2 LD50) group. PMC16 0.2 reduced cardiac cells LPO and ROS of Mal-exposed animals rather than that of MgSO4. PMC16 0.2 was also significantly better than MgSO(4) in improving MAL-induced changes in
ADP/
ATP ratio and also intracellular Mg levels. This study illustrates that
malathion-induced cardiac cells toxicity is improved by administration of Mg as a result of increasing cardiac
ATP through active transport of Mg inside the cells. Finally, the results of this study support positive effects of this magnetic Mg nanoparticle carrier but do not confirm its absolute efficacy that remains to be explored by further tests in different animal models and organs before moving to a phase I human trial.