Mercury can exist as a metallic element, inorganic salt, and organic compound. The form that is most associated with teratogenicity is the organic form. More specifically, methylmercury is the organic form of mercury that results in teratogenic effects when exposed to developing embryos. Methylmercury synthesis occurs when bacteria interact with the metallic mercury present in the sediments found in bodies of water. The methylmercury then accumulates to very high concentrations within the tissues of the aquatic animals, like fish, which are then consumed by humans. Because methylmercury is capable of easily crossing the placenta, the major route of embryo exposure to methylmercury is through consumption of these contaminated animals by the mother (Trasande, Landrigan, & Schechter, 2005).
Methylmercury is classified as a neurotoxicant due to resulting damage of the central nervous system and is one of the six most dangerous chemicals in the world’s environment, according to the International Program of Chemical Safety. Several studies have shown evidence that the effects of fetal exposure to methylmercury are much more severe than childhood or adult exposure. Furthermore, when a fetus shows adverse effects to mercury exposure, the mother very rarely shows any sign of being affected. The brains of infants and animals exposed to methylmercury in utero exhibit many differences when compared to brains that have developed under normal conditions. Neuronal migration and distribution patterns appear to be significantly affected when exposed to methylmercury in utero. Additionally, cell loss, reduced brain size, and brain scarring can be observed. Several hypotheses attempt to explain the differences in the appearance of the brain and include intracellular cytoskeletal structure rearrangements, increased reactive oxygen species (ROS), alterations of membrane function and signal transduction, decreased production of proteins, and shifts in neurotransmission (Gilbert & Grant-Webster, 1995). The images below display a couple of these hypotheses. Figure 1 looks at how methylmercury exposure can disrupt cytoskeletal structures within neurons, which in turn affects signal transduction and neurotransmission. Figure 2 shows a study conducted by Ni et al. (2010) in which the relationship between methylmercury exposure and ROS production was examined in the living microglial cells of rats.