Effect of oral methyl-t-butyl ether (MTBE) on the male mouse reproductive tract and oxidative stress in liver.
Effect of oral methyl-t-butyl ether (MTBE) on the male mouse reproductive tract and oxidative stress in liver.
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DOI：
10.1016/j.reprotox.2008.08.009
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发表时间：
2008-11
期刊：
影响因子：
--
通讯作者：
Klaunig JE
中科院分区：
文献类型：
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作者：
de Peyster A;Rodriguez Y;Shuto R;Goldberg B;Gonzales F;Pu X;Klaunig JE
MTBE存在于饮用水和其他用途的供水中。这些实验是对雄性小鼠口服MTBE后生殖道改变的早期报告的后续研究，并探讨了氧化应激作为一种作用模式。CD-1小鼠在第1、3和5天灌胃400-2000 mg/kg MTBE，在第6天ip注射hCG（2.5 IU/g），并在第7天尸检。睾丸组织学或睾酮水平无影响。使用类似的给药方案，其他人最初报告了MTBE灌胃小鼠的曲细精管破坏，尽管后来发表的结论与我们的发现一致。另一组还报告称，雄性BALB/c小鼠在饮用水中暴露于80-8000微克/毫升甲基叔丁基醚28天后，睾丸和其他生殖系统出现异常。我们将这些MTBE浓度给予成年小鼠28天，幼年小鼠51天，直至PND 77。使用MDA、TEAC和8 OH 2 hG作为终点，在幼龄研究的肝匀浆中检查氧化应激的证据。在所检查的水平下，甲基叔丁基醚暴露表明雄性小鼠生殖道没有显著变化，也没有肝脏氧化应激的迹象。这似乎是第一次口服MTBE暴露的幼年动物，也是第一次检查潜在的MTBE导致体内氧化应激使用一个典型的人体暴露途径。
MTBE is found in water supplies used for drinking and other purposes. These experiments follow up on earlier reports of reproductive tract alterations in male mice exposed orally to MTBE and explored oxidative stress as a mode of action. CD-1 mice were gavaged with 400–2000 mg/kg MTBE on days 1, 3, and 5, injected ip with hCG (2.5 IU/g) on day 6, and necropsied on day 7. No effect was seen in testis histology or testosterone levels. Using a similar dosing protocol, others had initially reported disruption of seminiferous tubules in MTBE–gavaged mice, although later conclusions published were consistent with our findings. Another group had also reported testicular and other reproductive system abnormalities in male BALB/c mice exposed for 28 days to 80–8000 ug/ml MTBE in drinking water. We gave these MTBE concentrations to adult mice for 28 days and juvenile mice for 51 days through PND 77. Evidence of oxidative stress was examined in liver homogenates from the juvenile study using MDA, TEAC and 8OH2hG as endpoints. MTBE exposures at the levels examined indicated no significant changes in the male mouse reproductive tract and no signs of hepatic oxidative stress. This appears to be the first oral MTBE exposure of juvenile animals, and also the first to examine potential for MTBE to cause oxidative stress in vivo using a typical route of human exposure.