Cadmium treatment induces echinocytosis, DNA damage, inflammation, and apoptosis in cardiac tissue of albino Wistar rats

Cadmium (Cd), a potent carcinogen present in almost all foods, poses a major health risk to humans. Major routes of exposure to Cd for humans are occupation, diet, and tobacco use. Cd elicits various deleterious effects on cellular molecules mainly by causing oxidant-antioxidant imbalance. Cd has been implicated in the pathogenesis of many cancers, Itai-itai disease, diabetic nephropathy, hypertension, peripheral artery disease, and myocardial infarction. This study was designed to investigate the effects of Cd intake on erythrocytes and cardiac tissue in male albino Wistar rats. We treated male albino Wistar rats with cadmium chloride (CdCl2) by intra-gastric administration for 30 days and examined Cd burden and changes in blood constituents and antioxidant status of blood and cardiac tissue. We also studied the structural alterations in the erthrocytes, elemental changes and Cd burden in cardiac tissue using scanning electron microscope (SEM/EDX). Inflammation and apoptosis were analysed in the cardiac tissue by polymerase chain reaction (PCR), western blotting, and DNA fragmentation assay. Cd treatment resulted in echinocytosis of erythrocytes and distorted myofibrils arrangement, vacuolization and congestion in the vessels. Cd administration has also induced inflammation and apoptosis in the cardiac tissue. At molecular level, Cd administration caused oxidative damage to DNA, lipids, and proteins and diminished the activities of various antioxidants. The present study provides a compelling evidence of Cd-induced imbalance in oxidant-antioxidant system with damage to erythrocytes and cardiac tissue that may contribute to various cardiac diseases.