Cadmium Toxicity: Oxidative Stress and Organ Dysfunction

Due to continued anthropogenic mobilization, cadmium accumulation in the environment causes various health problems because of its diverse toxic effects, extremely lingering biological half life (20–30 years), low rate of excretion from the body and storage predominantly in soft tissue primarily liver and kidney. Cadmium is known to have numerous noxious effects, including nephrotoxicity, hepatoxicity, osteoporosis, cardiovascular toxicity, lung toxicity, and reproductive toxicity. The biologically significant ionic form of cadmium, Cd 2+ , binds to many bio-molecules and these interactions underlie the toxicity mechanisms of cadmium. Some of the molecules (Mg 2+ , Ca 2+) and transition metal ions (e.g., Zn 2+ , Cu 2+ , Fe 3+/2+ ) is particularly sensitive to the presence of Cd 2+ because they enclose cationic sites to which the toxic metal can bind. Alterations in reactive oxygen species ( ROS) production during chronic exposures are less significant compared to the acute cadmium toxicity probably due to induced adaptation mechanism such as metallothionein and glutathione which in turn diminish cadmium induced oxidative stress. Many low molecular weight antioxidants (ascorbic acid, vitamin E, glutathione, Flavonoids) and other antioxidants are capable of chelating cadmium ions reducing their catalytic activity to form ROS. This mini review focused on direct evidence on cadmium induced ROS production, how different organ system responds to cadmium stress and pathological outcomes. For the treatment of cadmium intoxications a therapy with chelating agents has been applied. A better understanding of cadmium toxicity to tackle the environmental challenges lying ahead thus requires properly designed studies implementing biologically relevant cadmium concentrations on different cell types and use of these data in a theoretical framework integrating all cellular aspects of cadmium effects. Keywords : Cadmium, Oxidative stress, Antioxidant, ROS, Chelation