Ono B, Ishii N, Fujino S, Aoyama I
Laboratory of Environmental Hygiene Chemistry, Faculty of Pharmaceutical Sciences, Okayama University, Japan.
Appl Environ Microbiol. 1991 Nov;57(11):3183-6. doi: 10.1128/aem.57.11.3183-3186.1991.
Methylmercury-resistant mutants were obtained from Saccharomyces cerevisiae. They were divided into two complementation groups, met2 (homoserine O-acetyltransferase deficiency) and met15 (enzyme deficiency unknown), as reported previously. It was found that met15 was allelic to met17 (O-acetylserine and O-acetylhomoserine sulfhydrylase deficiency). Methylmercury toxicity was counteracted by exogenously added HS-, and both met2 and met17 (met15) mutants overproduced H2S. On the basis of these results, we conclude that met2 and met17 (met15) cause accumulation of hydrosulfide ions in the cell and that the increased level of hydrosulfide is responsible for detoxification of methylmercury.
从酿酒酵母中获得了抗甲基汞突变体。如先前报道,它们被分为两个互补组,即met2(高丝氨酸O - 乙酰转移酶缺陷)和met15(酶缺陷未知)。发现met15与met17(O - 乙酰丝氨酸和O - 乙酰高丝氨酸巯基化酶缺陷)等位。外源添加的HS - 可抵消甲基汞的毒性,并且met2和met17(met15)突变体均过量产生H2S。基于这些结果,我们得出结论,met2和met17(met15)导致细胞中氢硫化物离子积累,并且氢硫化物水平的升高是甲基汞解毒的原因。