Wild L G, Ortega H G, Lopez M, Salvaggio J E
Department of Medicine, Tulane University Medical School, New Orleans, Louisiana 70112, USA.
Environ Res. 1997;74(1):34-42. doi: 10.1006/enrs.1997.3748.
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 micrograms/liter of methyl mercury chloride (CH3HgCl) or 5 micrograms/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.
甲基汞是一种公认的健康危害物。它是一种在食物链中蓄积的环境污染物。人类接触汞的主要来源是食用受污染的鱼类。我们研究了间接接触甲基汞对斯普拉格 - 道利大鼠免疫系统的影响。在6周龄和12周龄的斯普拉格 - 道利大鼠中研究了不同形式的甲基汞对免疫系统发育的影响。通过在饮用水中给怀孕大鼠分别喂食5或500微克/升的氯化甲基汞（CH3HgCl）或5微克/升的硫化甲基汞[（CH3Hg）2S]，使大鼠在妊娠和哺乳期间间接接触汞。测量了子代大鼠的全身、脾脏和胸腺重量，并评估了自然杀伤（NK）细胞的溶细胞活性以及对T和B细胞有丝分裂原的淋巴细胞增殖反应。在6周龄时，高剂量和低剂量氯化甲基汞暴露组的全身和脾脏重量均显著增加。暴露于硫化甲基汞的大鼠在6周龄时胸腺重量显著增加。在12周龄时，全身和器官重量与对照组无差异。在6周龄时，两个氯化甲基汞暴露组的脾细胞对美洲商陆有丝分裂原（PWM）的淋巴细胞增殖反应均增强，而在硫化甲基汞暴露组中未受影响。在6周龄时，两组的NK细胞活性均未受影响。在12周龄时，两个氯化甲基汞暴露组的NK细胞活性在统计学上显著降低了56.6%，而在硫化甲基汞暴露的大鼠中未受影响。氯化甲基汞组脾细胞对B细胞有丝分裂原商陆的淋巴细胞增殖反应仍然增强。大鼠在妊娠和哺乳期间间接接触不同形式的甲基汞表明，氯化物形式对脾细胞的淋巴细胞增殖反应主要有延长的增强作用，随后是NK细胞活性的显著降低。
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