Therapeutic Effect of Deferasirox and Glycine on Chronic Cadmium Toxicosis in Rats

Cadmium is a well recognized environmental pollutant with diverse toxicity in various organs of human and animals (IARC, 1993). Prolong cadmium exposures can cause lung fibrosis, kidney tubular dysfunction, hypertension, osteoporosis, cancer, etc. (Peters et al., 1986; Patra et al., 2011). The common sources of cadmium are combustion of coal, mining, smelters and contaminated phosphate fertilizers (Patra et al., 2005; Patra et al., 2007). Major occupational exposure occurs from nonferrous smelters during production and processing of cadmium (Patra et al., 2011). Cadmium was found to result in oxidative stress (Hendy et al., 1992; Somashekaraiah et al., 1992) by inducing oxygen free radical production (Balaknina et al., 2005; Demirevska et al., 2006; Dailiah Roopha et al., 2011). Cadmium causes oxidative damage to erythrocytes and various tissues by stimulating the formation of metallothioneins and reactive oxygen species (ROS) (Sarkar et al., 1998). Long term exposure to cadmium increases lipid peroxidation (LPO) and inhibits superoxide dismutase (SOD) activity, causing oxidative damage in liver, kidney and testis (Patra et al., 1999). The increase in lipid peroxidation due to cadmium toxicity have been attributed to alterations in the enzymatic antioxidant defense system such as glutathione peroxidase (GPH-Px), superoxide dismutase (SOD), and catalase (CAT) (Patra et al., 2011). Thus, cadmium toxicosis treatment should consist of cadmium chelation and free radical scavenging.