萘醌类刺激人体微粒体对六价铬的还原速率

C. Myers, B. Porgilsson, B. P. Carstens, J. Myers
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引用次数: 2

摘要

在厌氧条件下,1,4-萘醌(NQ)或2-甲基-1,4-萘醌(MNQ)显著刺激了人肝微粒体对已知致癌物铬(VI)的nadph依赖性还原。当醌浓度从1 μ m增加到5 μ m时,刺激最明显。另外,在5 μ m以上,随着醌浓度的增加,出现了较小的增加。这些醌类化合物还引起人体肺微粒体对铬(VI)还原的明显刺激。偶氮和硝基芳香族化合物,以及甲基紫剂(百草枯)似乎没有什么影响。由于明显的刺激发生在NQ和MNQ水平远低于初始铬(VI)浓度时,醌可能通过它们的半醌自由基进行氧化还原循环,而这些自由基可能正在还原铬(VI)。为了支持这一现象,NQ和MNQ在有氧条件下引起NADPH消耗的显著刺激,其中t…
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NAPHTHOQUINONES STIMULATE THE RATE OF REDUCTION OF HEXAVALENT CHROMIUM BY HUMAN MICROSOMES
The NADPH-dependent reduction of chromium (VI), a known carcinogen, by human hepatic microsomes was significantly stimulated by 1,4-naphthoquinone (NQ) or 2-methyl-1,4-naphthoquinone (MNQ) under anaerobic conditions. The most pronounced stimulation occurred when quinone concentrations were increased from 1 to 5 muM. Additional, but smaller, increases were seen with subsequent increases in quinone concentration above 5 muM. These quinones also caused pronounced stimulation of chrom ium(VI) reduction by human lung microsomes. Azo and nitroaromatic compounds, as well as methylviologen (Paraquat), seemed to have little effect. Since marked stimulation occurred with levels of NQ and MNQ that were well below those of the initial chromium(VI) concentration, the quinones probably are being redox-cycled through their semiquinone radicals, and these radicals probably are reducing chromium(VI). In support of this occurrence, NQ and MNQ caused a marked stimulation of NADPH consumption under aerobic conditions, with t...
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