Cardiotoxic Effects of Manganese Chloride in Albino Rats

Abstract

Manganese (Mn) is an essential trace element required for normal physiological function, but excessive exposure has been associated with toxic effects on several organ systems, including the cardiovascular system. While the neurotoxic effects of manganese are well documented, less attention has been paid to its direct effects on cardiac tissue. This study investigated the cardiotoxic role of manganese chloride (MnCl) in albino Wistar rats and evaluated the protective potential of the ethanolic extract of Cocos nucifera husk by assessing oxidative stress biomarkers in heart tissue, namely malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD). Forty (40) adult male Wistar rats were randomly allocated into four groups of ten animals each: a normal control group (Group A); a group administered MnCl alone at 714 µg/kg body weight for 21 days (Group B); a group administered MnCl (714 µg/kg) concurrently with ethanolic extract of Cocos nucifera husk (250 mg/kg) for 21 days (Group C); and a group administered MnCl (714 µg/kg) for 21 days followed by the extract alone (250 mg/kg) for a further 15 days (Group D). Cardiac MDA, catalase, and SOD were determined spectrophotometrically. Results show that MnCl administration (Group B) produced a significant increase in cardiac MDA concentration alongside significant reductions in catalase and SOD activities relative to the control group (p<0.05), consistent with manganese-induced oxidative damage to the myocardium. Co-administration of the extract, whether concurrently or as a post-exposure recovery treatment, significantly attenuated these changes. These findings support the hypothesis that oxidative stress is a central mechanism underlying manganese-induced cardiotoxicity in albino rats, and highlight the heart as a tissue vulnerable to manganese-induced redox imbalance, an effect that has received comparatively little attention relative to its neurotoxic profile.