The Effects of Methylmercury on Mitochondrial Function and Reactive Oxygen Species Formation in Rat Striatal Synaptosomes Are Age-Dependent

New York State Department of Health, Wadsworth Center, Albany, New York, 12201, USA.
Toxicological Sciences (Impact Factor: 3.85). 10/2005; 87(1):156-62. DOI: 10.1093/toxsci/kfi224
Source: PubMed


Methylmercury (MeHg) is especially toxic to the developing central nervous system. In order to understand the reasons for this age-dependent vulnerability, we compared the effects of MeHg on formation of reactive oxygen species (ROS) and mitochondrial function in striatal synaptosomes obtained from rats of various ages. Basal ROS levels were greater, and basal mitochondrial function was lower, in synaptosomes from younger animals, compared to adult animals. MeHg induced ROS formation in synaptosomes from rats of all ages, although the increases were greatest in synaptosomes from the younger animals. MeHg also reduced mitochondrial metabolic function, as assessed by MTT reduction, as well as mitochondrial membrane potential; again, the greatest changes were seen in synaptosomes from early postnatal animals. These age-dependent differences in susceptibility to MeHg are most likely due to a less efficient ROS detoxifying system and lower activity of mitochondrial enzymes in tissue from young animals.

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    • "A number of mechanisms have been proposed to be involved in MeHg toxicity, including alterations in calcium homeostasis (Komulainen and Bondy, 1987; Marty and Atchison, 1997) and apoptosis/necrosis (Kunimoto, 1994). Additionally, in the recent years, several studies have implicated the formation of reactive oxygen species (ROS) (Yee and Choi, 1994, 1996; Dreiem et al., 2005) and disruption of mitochondrial function (Hare and Atchison, 1992; Limke and Atchison, 2002) as two key mechanisms in MeHg-induced toxicity. Previously, Ali et al. (1992) reported increased rates of formation of ROS in methylmercury-treated rats. "
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