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首页> 外文期刊>Archives of Toxicology >Quantification of individual glutathione S-transferase isozymes in hepatic and pulmonary tissues of naphthalene-tolerant mice.
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Quantification of individual glutathione S-transferase isozymes in hepatic and pulmonary tissues of naphthalene-tolerant mice.

机译：萘耐受小鼠肝和肺组织中个别谷胱甘肽S-转移酶同工酶的定量。

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Acute exposure to naphthalene produces severe bronchiolar epithelial cell necrosis in mice, whereas subchronic exposure to naphthalene (200 mg/kg/7 days) fails to produce epithelial necrosis and renders the animals tolerant to subsequent challenge doses of naphthalene. Mechanisms responsible for the development of tolerance have not been delineated. The few studies exploring naphthalene tolerance focus on expression of microsomal enzymes and have yet to delve into expression of the hepatic detoxification enzymes such as glutathione S-transferases (GSTs; EC 2.5.1.18). Glutathione conjugation catalyzed by GSTs accounts for one of the two primary routes of naphthalene detoxification. In this study, we rigorously quantify levels of individual GST isozymes expressed within the livers and lungs of mice with acquired tolerance to naphthalene. Subchronic exposure to naphthalene increases the abundance of some hepatic GSTs to levels as much as 68% greater than controls. Naphthalene-tolerant mice displayed increases in mGSTM1 (51%), mGSTM2 (58%), and mGSTP1 (66%), whereas no significant difference in mGSTA3 was observed between exposed and control mice. Extracts of pulmonary tissues from naphthalene-tolerant mice showed minor increases in levels of mGSTP1 (7%) and Peak 8 isozyme (27%) and decreases in levels of mGSTM1 (31%), mGSTM2 (17%), and mGSTA3 (8%). The total enzymatic activity for the conjugation of 1-chloro-2,4-dinitrobenzene (CDNB) was 22% lower in lung extracts from naphthalene-tolerant animals than in controls. These results indicate that induction of hepatic GSTs is substantial and may be an important factor in the development of tolerance to naphthalene.
机译：急性暴露于萘会在小鼠中引起严重的细支气管上皮细胞坏死，而亚慢性暴露于萘（200 mg / kg / 7天）则不会产生上皮坏死，并使动物对随后的萘挑战剂量耐受。尚未描述引起耐受性增加的机制。几项探索萘耐受性的研究侧重于微粒体酶的表达，但尚未深入研究肝脏解毒酶（如谷胱甘肽S-转移酶（GSTs; EC 2.5.1.18））的表达。 GST催化的谷胱甘肽结合是萘解毒的两个主要途径之一。在这项研究中，我们严格量化了对萘具有耐受性的小鼠肝脏和肺中表达的个别GST同工酶的水平。亚慢性暴露于萘会使某些肝脏GST的丰度比对照组高68％。耐萘的小鼠在mGSTM1（51％），mGSTM2（58％）和mGSTP1（66％）中显示增加，而在暴露的小鼠和对照小鼠之间未观察到mGSTA3的显着差异。耐萘的小鼠的肺组织提取物显示mGSTP1（7％）和Peak 8同工酶（27％）的含量略有增加，而mGSTM1（31％），mGSTM2（17％）和mGSTA3（8％的含量）降低）。与萘相比，耐萘动物肺提取物中1-氯-2,4-二硝基苯（CDNB）结合的总酶活性低22％。这些结果表明，肝GST的诱导是实质性的，并且可能是对萘耐受性发展的重要因素。

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