Academic journal article Environmental Health Perspectives

Methylmercury Pause: Study Suggests Long Latency for Neurotoxicity

Academic journal article Environmental Health Perspectives

Methylmercury Pause: Study Suggests Long Latency for Neurotoxicity

Article excerpt

Methylmercury (MeHg) easily crosses the blood-brain barrier and accumulates in the central nervous system, where it is demethylated to inorganic mercury. Chronic perinatal exposure to environmentally relevant levels of MeHg is associated with the occurrence later in childhood of neurobehavioral problems such as impaired attention and fine motor function. Animal studies confirm this association, but epidemiologic evidence is mixed despite extensive study. Moreover, MeHg toxicity and the period of time before effects appear are not completely understood, as few studies have been conducted beyond the first months or years of life in either animals or humans. Researchers now demonstrate in a mouse model that effects from early exposure to methylmercury can occur years after early-life mercury levels in the brain have declined [EHP 116: 746-751; Yoshida et al.].

In the current study, investigators used two strains of mice--the wild-type C57BL strain and the genetically manipulated metallo-thionein (MT)-null strain. The latter was used to examine potential genetic susceptibility to the toxic effects of MeHg exposure, as MT-null mice do not produce metallothionein-I and II proteins that can bind metals and protect against their toxic effects. Mice were exposed through diet to low levels of MeHg (5[micro]g/g diet) from the first day of pregnancy through the tenth day after birth. Offspring of the treated mice were weaned at 28 days. At 12 and 52 weeks (roughly comparable to young adulthood and middle age in humans), the offspring underwent behavioral tests of their locomotor activity and learning ability. …

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