Heavy Metal Carcinogenesis: A Possible Mechanistic Role for Apoptosis
Post-doctoral fellow, President and Primary Biochemist, Moondust Cosmetics Ltd., Canada
*Corresponding author: Chanda Siddoo-Atwal, Post-doctoral fellow, President and Primary Biochemist, Moondust Cosmetics Ltd., Canada, E-mail: firstname.lastname@example.org
The term “heavy metals” refers to naturally occurring elements in the periodic table with relatively high densities (at least 5 times greater than water), atomic weights, or atomic numbers. Certain heavy metals such as lead, mercury, and chromium are highly poisonous to humans. In fact, metal pollution is a serious environmental problem of the present-day. It occurs as a result of various commercial activities including the mining and smelting of metalliferous ores, electroplating, gas exhaust, energy and fuel production, fertilizer and pesticide application (Alkorta I et al, 2004). Moreover, heavy metals have multiple industrial, domestic, agricultural, medical and technological applications. These metallic elements are highly toxic and can induce multiple organ damage even at relatively low levels of exposure. Many are classed as known or probable carcinogens. However, some of the mechanistic aspects of heavy metal carcinogenesis are not clearly understood (Tchounwou PB et al, 2012). Lead, mercury, and chromium have all been associated with an elevation in activity of cellular apoptotic or oxidative stress pathways, which can result in apoptosis. Both lead and mercury can cause metabolic perturbations by altering intracellular calcium levels in mitochondria resulting in cell death. Chromium can also cause mitochondrial- stimulated and p53-dependent apoptosis in cells. An increase in the basal frequency of apoptotic cell death in animal and human models has been linked to carcinogenesis (Siddoo- Atwal C, 2009). This paper focuses on the possible role of the stimulation of apoptotic mechanisms in heavy metal carcinogenesis based on the experimental effects of these metals.