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本文引用的文献

1
The effects of methyl tert-butyl ether (MTBE) on the male rat reproductive system.甲基叔丁基醚(MTBE)对雄性大鼠生殖系统的影响。
Food Chem Toxicol. 2008 Jul;46(7):2402-8. doi: 10.1016/j.fct.2008.03.024. Epub 2008 Apr 3.
2
Methyl tert-butyl ether (MTBE)-induced cytotoxicity and oxidative stress in isolated rat spermatogenic cells.甲基叔丁基醚(MTBE)对离体大鼠生精细胞的细胞毒性和氧化应激作用。
J Appl Toxicol. 2007 Jan-Feb;27(1):10-7. doi: 10.1002/jat.1178.
3
Methyl tertiary-butyl ether mode of action for cancer endpoints in rodents.
Regul Toxicol Pharmacol. 2007 Mar;47(2):156-65. doi: 10.1016/j.yrtph.2006.09.003. Epub 2006 Nov 3.
4
Absence of acute testicular toxicity of methyl-tert butyl ether and breakdown products in mice.
Bull Environ Contam Toxicol. 2005 Aug;75(2):228-35. doi: 10.1007/s00128-005-0742-8.
5
The mutagenicity testing of tertiary-butyl alcohol, tertiary-butyl acetate and methyl tertiary-butyl ether in Salmonella typhimurium.叔丁醇、乙酸叔丁酯和甲基叔丁基醚在鼠伤寒沙门氏菌中的致突变性测试。
Mutat Res. 2005 Jan 3;565(2):181-9. doi: 10.1016/j.mrgentox.2004.10.002.
6
Determination of malondialdehyde by liquid chromatography as the 2,4-dinitrophenylhydrazone derivative: a marker for oxidative stress in cell cultures of human hepatoma HepG2.通过液相色谱法测定作为2,4-二硝基苯腙衍生物的丙二醛:人肝癌HepG2细胞培养物中氧化应激的标志物
J Chromatogr B Analyt Technol Biomed Life Sci. 2004 Jun 5;805(1):33-9. doi: 10.1016/j.jchromb.2004.02.004.
7
Subchronic studies in Sprague-Dawley rats to investigate mechanisms of MTBE-induced Leydig cell cancer.在斯普拉格-道利大鼠中进行的亚慢性研究,以探究甲基叔丁基醚诱导睾丸间质细胞瘤的机制。
Toxicol Sci. 2003 Mar;72(1):31-42. doi: 10.1093/toxsci/kfg011.
8
The paradoxes ofMTBE.
Toxicol Sci. 2001 Jun;61(2):211-7. doi: 10.1093/toxsci/61.2.211.
9
Measurement of free and bound malondialdehyde in plasma by high-performance liquid chromatography as the 2,4-dinitrophenylhydrazine derivative.通过高效液相色谱法测定血浆中作为2,4-二硝基苯肼衍生物的游离和结合丙二醛。
J Chromatogr B Biomed Sci Appl. 2000 Jun 9;742(2):315-25. doi: 10.1016/s0378-4347(00)00174-2.
10
Alterations in endocrine responses in male Sprague-Dawley rats following oral administration of methyl tert-butyl ether.雄性斯普拉格-道利大鼠口服甲基叔丁基醚后内分泌反应的变化。
Toxicol Sci. 2000 Mar;54(1):168-76. doi: 10.1093/toxsci/54.1.168.

口服甲基叔丁基醚(MTBE)对雄性小鼠生殖道及肝脏氧化应激的影响。

Effect of oral methyl-t-butyl ether (MTBE) on the male mouse reproductive tract and oxidative stress in liver.

作者信息

de Peyster Ann, Rodriguez Yvonne, Shuto Rika, Goldberg Beck, Gonzales Frank, Pu Xinzhu, Klaunig James E

机构信息

Graduate School of Public Health, San Diego State University, San Diego, CA 92182, United States.

出版信息

Reprod Toxicol. 2008 Nov-Dec;26(3-4):246-53. doi: 10.1016/j.reprotox.2008.08.009. Epub 2008 Sep 9.

DOI:10.1016/j.reprotox.2008.08.009
PMID:18824092
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4574623/
Abstract

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 i.p. 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 microg/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.

摘要

甲基叔丁基醚存在于用于饮用和其他用途的水源中。这些实验是对早期关于经口暴露于甲基叔丁基醚的雄性小鼠生殖道改变的报告的后续研究,并探讨了氧化应激作为一种作用方式。在第1、3和5天,给CD-1小鼠灌胃400 - 2000毫克/千克甲基叔丁基醚,在第6天腹腔注射人绒毛膜促性腺激素(2.5国际单位/克),并在第7天进行尸检。在睾丸组织学或睾酮水平方面未观察到影响。使用类似的给药方案,其他人最初报告在灌胃甲基叔丁基醚的小鼠中曲细精管受到破坏,尽管后来发表的结论与我们的发现一致。另一组也报告了雄性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天的睾丸及其他生殖系统异常。我们将这些甲基叔丁基醚浓度给予成年小鼠28天,给予幼年小鼠直至出生后第77天共51天。在幼年研究中,以丙二醛、总抗氧化能力和8-羟基脱氧鸟苷为指标,检测肝脏匀浆中的氧化应激证据。在所检测的甲基叔丁基醚暴露水平下,雄性小鼠生殖道未出现显著变化,也没有肝脏氧化应激的迹象。这似乎是首次对幼年动物进行口服甲基叔丁基醚暴露实验,也是首次使用人类典型暴露途径研究甲基叔丁基醚在体内引起氧化应激的可能性。