Immune System Alteration in the Rat after Indirect Exposure to Methyl Mercury Chloride or Methyl Mercury Sulfide

Abstract

Methyl mercury is a well-recognized health hazard. It is an environmental contaminant that accumulates in the food chain. The primary source of mercury exposure for humans is through the consumption of contaminated fish. We studied the effects of indirect methyl mercury exposure on the immune system of Sprague–Dawley rats. The effects of different forms of methyl mercury on immune system development were studied in Sprague–Dawley rats at 6 and 12 weeks of age. Rats were indirectly exposed to mercury during gestation and during nursing by exposing pregnant rats to either 5 or 500 μg/liter of methyl mercury chloride (CH3HgCl) or 5 μg/liter of methyl mercury sulfide [(CH3Hg)2S] in their drinking water. Total body, splenic, and thymic weights were measured, and NK cell cytolytic activity and lymphoproliferative response to T and B cell mitogens were evaluated in the offspring. At 6 weeks of age, total body and splenic weights were significantly increased in both high- and low-dose methyl mercury chloride-exposed groups. Rats exposed to methyl mercury sulfide had a significant increase in thymic weight at 6 weeks of age. At 12 weeks, the total body and organ weights were not different from controls. The lymphocyte proliferative response of splenocytes to PWM was enhanced at 6 weeks in both CH3HgCl exposed groups and not affected in the (CH3Hg)2S exposed group. NK cell activity was not affected in either group at 6 weeks of age. At age 12 weeks, NK cell activity was statistically significantly decreased by 56.6% in both CH3HgCl-exposed groups and not affected in the (CH3Hg)2S-exposed rats. The lymphocyte proliferative response of splenocytes to the B cell mitogen pokeweed remained increased in the CH3HgCl groups. Indirect exposure of rats (during gestation and nursing) to different forms of methyl mercury reveals that chloride forms have prolonged predominantly enhancing effects on lymphoproliferative response of splenocytes, followed by significant depression of NK cell activity.