egarding the potential interrelation between lead (Pb) toxicity and cardiovascular diseases, the current investigation aims to study the alterations of some metabolic enzyme activities as well as oxidative stress-related parameters in the myocardium of lead-exposed mice. Twelve male mice are distributed arbitrarily into two equal groups. First group served as control. Mice in group 2 received water containing 1000 mg L−1 lead acetate. The results revealed that Pb-treated mice had significantly higher values of cardiac troponin I and creatine kinase MB as compared with the control group. Moreover, Pb-treated mice had comparatively lower values of cardiac superoxide dismutase, catalase, and glutathione. Considerable rise of cardiac lactate dehydrogenase and alanine aminotransferase as well as malondialdehyde was also detected in Pb-exposed group. However, the influences of lead poisoning on other measured indices including protein carbonyls, ferric reducing antioxidant power, glutathione peroxidase, alkaline phosphatase, and aspartate aminotransferase were not significant compared with controls. The current data show that lead exposure in mice results in histochemical disturbances in heart tissue which are manifested by decreased quantities of some endogenous antioxidants, increased levels of lipid peroxidation and some enzyme activities, as well as increase of measured plasma indices of cardiac damage. These findings suggested that some biological systems of heart tissue can be influenced following Pb exposure which should be considered in the pathogenesis of Pb-induced cardiac toxicity.

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