Abstract

Reactive oxygen species (ROS) include such chemical moieties as superoxide anion (O2 −), hydrogen peroxide (H2O2), hydroxyl radical (HO−), and peroxynitrite (ONOO−) Boelsterli 2003. ROS are formed as a natural by-product of the normal metabolism of oxygen and has important roles in cell signaling. However, during times of environmental stress, ROS levels can increase dramatically, which can result in significant damage to cell structures. This cumulates into a situation known as oxidative stress. They are also generated by exogenous sources such as ionizing radiations. In humans, oxidative stress is involved in many diseases, such as atherosclerosis, Parkinson’s disease, and Alzheimer’s disease, but it may also be important in prevention of aging by induction of a process named mitohormesis. Reactive oxygen species can be beneficial, as they are used by the immune system as a way to attack and kill pathogens. Though ROS are produced at a basal level by the mitochondrial respiratory chain and in cytochrome p450 (CYP)-mediated oxidation processes (Boelsterli 2003), cells have endogenous antioxidants (e.g., cytochrome oxidase, superoxide dismutases, catalases, peroxidases, and glutathione, to name a few) as a means to control these substances (Buonocore et al. 2001). Certain disease states as well as pathologies resulting from toxic substances, including methylmercury, produce ROS in numbers that can overwhelm the cellular defense mechanisms and result in oxidative stress. The ROS can damage vital cellular molecules such as DNA, proteins, and lipids. Since ROS can also play a role via redox signaling in the regulation of signal transduction (Suzuki et al. 1997), excess production of these substances may prove lethal to the cell. Methylmercury-induced production of ROS will be addressed in more depth subsequently.

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