Published Paper Details:

Metal compounds that are carcinogenic and harm human health through occupational and environmental exposure include arsenic, cadmium, chromium, cobalt, lead, mercury, and nickel. However, the fundamental processes leading to tumor development remain poorly understood. Oxidative stress, which is a discrepancy between the system's capacity to quickly detoxify reactive intermediates and the rate at which free radicals are produced, may be caused by interference with metal homeostasis. As a result, this incident results in protein modification, lipid peroxidation, DNA damage, and maybe symptoms of numerous diseases, including cancer. Numerous molecular markers and common mechanisms of action are included in this overview. Free radicals produced by metals, oxidative stress, protein, lipid, and DNA damage, responsive signal transduction pathways important for cell growth and development, and the functions of antioxidant enzymes and DNA repair systems are all discussed. It is also discussed how certain regulatory factors, such as AP-1, NF-B, Ref-1, and p53, interact with non-enzymatic antioxidants, such as carotenoids, flavonoids, glutathione, selenium, vitamin C, and vitamin E. Cellular oxidative stress markers, such as catalase, glutathione peroxidase, and superoxide dismutase, are also discussed. Oncogenic stimulation is associated with dysregulation of defensive mechanisms, including the cellular antioxidant network against free radicals and a deficit in DNA repair. These findings support the hypothesis that DNA repair proteins and newly developing regulatory factors responsive to oxidative stress serve as possible predictors of tumor initiation and progression.