Friedman M A, Eaton L R, Bailey W
Bull Environ Contam Toxicol. 1978 Jul;20(1):102-10. doi: 10.1007/BF01683493.
The influence of environmental or dietary factors on the toxicity of methylmercury (MeHg) was investigated due to possibilities that humans exposed to methylmercury may have been sensitized. Groups of 8 rats were exposed to 0, 20 or 40 ppm MeHg in a semisynthetic diet and fed 0.5% BHT, 5% protein (instead of 15%), or injected with 250 mg/kg CC14 or acetaldehyde. In control rats neurotoxicity occurred at 4 weeks and 9 weeks with 40 and 20 ppm MeHg, respectively. Mortality was observed at 6 weeks with 40 ppm and 1 rat died in week 9 with 20 ppm MeHg. Acetaldehyde injected rats died at week 4 and 6 when fed 40 or 20 ppm MeHg. Neurotoxicity was observed in week 3 and 5 in these groups, respectively. Treating rats with the low protein or BHT accelerated neurotoxicity and mortality by 1 week with 40 ppm MeHg. These agents had killed all test animals within 7 weeks at 20 ppm MeHg. Neither acetaldehyde nor BHT influenced 0 ppm MeHg controls while 5% protein induced precipitous weight loss. In the case of CC14, the rats lived longer in combination experiments than one would have expected from the individual treatments.
由于接触甲基汞的人类可能已被致敏,因此研究了环境或饮食因素对甲基汞(MeHg)毒性的影响。将每组8只大鼠置于含0、20或40 ppm甲基汞的半合成饮食中,并喂食0.5%的丁基羟基甲苯(BHT)、5%的蛋白质(而非15%),或注射250 mg/kg的四氯化碳(CC14)或乙醛。在对照大鼠中,分别在4周和9周时,40 ppm和20 ppm甲基汞出现神经毒性。在40 ppm时,6周出现死亡,在20 ppm甲基汞时,有1只大鼠在第9周死亡。注射乙醛的大鼠在喂食40或20 ppm甲基汞时,分别在第4周和第6周死亡。在这些组中,分别在第3周和第5周观察到神经毒性。用低蛋白或BHT处理大鼠,可使40 ppm甲基汞的神经毒性和死亡率提前1周出现。在20 ppm甲基汞时,这些药物在7周内杀死了所有实验动物。乙醛和BHT对0 ppm甲基汞对照组均无影响,而5%的蛋白质导致体重急剧下降。在四氯化碳的情况下,在联合实验中大鼠的存活时间比单独处理时预期的要长。