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首页> 外文期刊>Journal of applied toxicology >Effect of beta-naphthoflavone and phenobarbital on the nephrotoxicity of chlorotrifluoroethylene and 1,1-dichloro-2,2-difluoroethylene in the rat.
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Effect of beta-naphthoflavone and phenobarbital on the nephrotoxicity of chlorotrifluoroethylene and 1,1-dichloro-2,2-difluoroethylene in the rat.

机译：β-萘黄酮和苯巴比妥对大鼠三氟氯乙烯和1,1-二氯-2,2-二氟乙烯的肾毒性的影响。

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The role of cytochrome P450 activity in the nephrotoxicity of chlorotrifluoroethylene (CTFE) and 1,1-dichloro-2,2-difluoroethylene (DCDFE) was investigated in the male rat. Hepatic cytochrome P450 1A1 and principally P450 2B1[sol ]2 were induced by beta-naphthoflavone and phenobarbital, respectively. Nephrotoxicity was evaluated by investigating urine biochemical parameters, kidney histochemistry and histopathological modifications.Both CTFE and DCDFE induce severe nephrotoxicity in rats after 4 h of exposure to 200 and 100 ppm, respectively. Compared with controls, activity levels of gamma-glutamyltranspeptidase (gammaGT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and N-acetyl-beta-d-glucosaminidase (NAG) in 24-h urine were increased similarly, but urinary excretion of glucose, proteins and beta(2)-microglobulin (beta(2)-m) and serum urea and creatinine levels were increased. Histopathological and histochemical examinations of kidney sections of CTFE- and DCDFE-exposed rats revealedcellular necrosis and tubular lesions 24 h after exposure.beta-Naphthoflavone-pretreated rats were afforded some protection against the nephrotoxicity of CTFE and DCDFE. Phenobarbital did not modify DCDFE nephrotoxicity but afforded some protection against CTFE nephrotoxicity. In conclusion, CTFE and DCDFE are strong nephrotoxins. Cytochrome P450 1A1 is implicated in CTFE and DCDFE metabolism and one or several cytochromes induced by phenobarbital are implicated in CTFE metabolism. The P450 cytochromes involved in CTFE and DCDFE metabolism probably constitute detoxication metabolic pathways. The nephrotoxicity of CTFE and DCDFE is therefore subordinated to the cytochrome P450 activity involved in their metabolism. Copyright (c) 2005 John Wiley & Sons, Ltd.
机译：在雄性大鼠中研究了细胞色素P450活性在三氟氯乙烯（CTFE）和1,1-二氯-2,2-二氟乙烯（DCDFE）的肾毒性中的作用。 β-萘黄酮和苯巴比妥分别诱导肝细胞色素P450 1A1和主要是P450 2B1 [sol] 2。通过研究尿液的生化参数，肾脏组织化学和组织病理学改变来评估肾毒性。CTFE和DCDFE分别暴露于200 ppm和100 ppm 4 h后，会引起大鼠严重的肾毒性。与对照组相比，24小时尿液中的γ-谷氨酰转肽酶（gammaGT），天冬氨酸转氨酶（AST），碱性磷酸酶（ALP）和N-乙酰基-β-d-氨基葡萄糖苷酶（NAG）的活性水平类似地增加，但尿液排泄葡萄糖，蛋白质和β（2）-微球蛋白（β（2）-m）和血清尿素和肌酐水平升高。暴露后24小时，对暴露于CTFE和DCDFE的大鼠的肾脏切片进行组织病理学和组织化学检查，发现细胞坏死和肾小管病变。β-萘黄酮预处理的大鼠对CTFE和DCDFE的肾毒性具有一定的保护作用。苯巴比妥并没有改变DCDFE的肾毒性，但提供了一定的抗CTFE肾毒性的保护。总之，CTFE和DCDFE是强肾毒素。细胞色素P450 1A1与CTFE和DCDFE代谢有关，而苯巴比妥诱导的一种或几种细胞色素与CTFE代谢有关。参与CTFE和DCDFE代谢的P450细胞色素可能构成了脱毒代谢途径。因此，CTFE和DCDFE的肾毒性服从于它们代谢中涉及的细胞色素P450活性。版权所有（c）2005 John Wiley＆Sons，Ltd.

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