In addition, decreased glucose levels and increased total lipid content in cardiac tissue of rats following cadmium exposure were observed. The decreased activities of alanine transaminase and aspartate transaminase reflected decreased metabolic protein degradation and increased lactate dehydrogenase activity. Since the metabolic pathways were altered by cadmium exposure, it can be concluded that Cd2+-induced formation of ROS initiates a series of events that occur in the heart Selleck GSK-3 inhibitor which in turn resulted

in alterations of metabolic pathways. The testis is a good marker of cadmium exposure. Cadmium-induced testicular damage and testicular necrosis have been documented by many reporters (see for example Dalton et al., 2005). Various studies have been performed on the cadmium-induced testicular toxicity in rat models. A significantly increased content of malondialdehyde and glutathione peroxidase (GSH-Px) in exposed groups has been observed (Yang et al., 2003). Glutathione was found to scavenge intracellular oxygen radicals either directly or via the GSH peroxidase/GSH system. The activity of superoxide dismutase in the tested animals was lowered. This study also revealed that the number of cells with DNA single strand breaks and the levels of cellular DNA damage

were significantly higher in exposed groups than in controls. Cadmium is a potent human carcinogen causing preferentially prostate, lung selleck inhibitor and Niclosamide gastro-intestinal (kidney and pancreas) cancers. Smoking synergistically increases the carcinogenic effect of cadmium (Flora et al., 2008 and Flora and Pachauri, 2010). The effect of environmental exposure to cadmium on cancer incidence (particularly that of the lung) in the environmentally contaminated north-east Belgium (the neighbourhood of zinc smelters) has been extensively investigated (Sartor et al., 1992). The results have shown an association between risk of cancer and cadmium exposure as shown by 24-h urinary excretion – a finding that remained consistent after adjustment for sex, age and smoking.

New findings in the explanation of cadmium-induced carcinogenicity with respect to cell adhesion have recently been published. E-cadherin, a transmembrane Ca(II)-binding glycoprotein playing an important role in cell–cell adhesion, can bind cadmium to Ca(II)-binding regions, changing the glycoprotein conformation (Pearson and Prozialeck, 2001). Thus the disruption of cell–cell adhesion induced by cadmium could play an important role in tumour induction and promotion. Intoxication with cadmium led to significantly increased concentration of lipid peroxides in rats and altered activity of antioxidant enzymes such as Cu, Zn-SOD, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase (Ognjanovic et al., 2003). Pretreatment with vitamin E revealed a protective role against the toxic effects of cadmium as substantiated by the hematological values of lipid peroxides.