Aim of the work: The present study was performed to determine the possible protective effects of erdosteine and exogenous reduced nicotinamide adenine dinucleotide phosphate (NADPH) against cardiotoxicity produced by aluminium phosphide (AlP) via measurement of serum cardiac markers and assessment of cardiomyocyte viability and apoptosis by flow cytometry analysis.
Material and methods: Fifty-four adult albino rats were divided into seven groups as follows; four control groups (negative control, solvent control, erdosteine control, NADPH control), AlP group (12 mg/kg) orally, AlP + erdosteine (150 mg/kg) orally, AlP + NADPH (16 mg/kg) intravenously. After 8 hours, blood samples were collected from the retro-orbital plexus for analysis of serum cardiac markers, and then the chest and abdomen were carefully incised to remove the hearts for flow cytometry analysis and histopathological examination.
Results revealed that AlP poisoning caused an increase in serum cardiac markers (LDH, cTnI) with a marked decrease in the viability of cardiac myocytes and a marked increase in the percent of apoptotic cardiac myocytes. Co-administration of erdosteine with AlP slightly improved serum cardiac markers and cardiomyocyte viability, with a slight decrease in the percent of apoptosis. Coadministration of NADPH with AlP showed marked improvement in serum cardiac markers, a marked increase in myocardial cell viability, and a marked decrease in the percent of apoptotic myocytes.
Conclusion: These findings were confirmed by histopathological examination of heart tissues from each group. From the previous data, it can be concluded that administration of exogenous NADPH intravenously may be a promising antidote for AlP toxicity.
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