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. 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. 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 |
