Xu Z, Kawai M, Bandiera S M, Chang T K
Food, Nutrition, and Health Program, The University of British Columbia, 2205 East Mall, V6T 1Z4, Vancouver, British Columbia, Canada.
Biochem Pharmacol. 2001 Nov 1;62(9):1283-91. doi: 10.1016/s0006-2952(01)00776-6.
The present study investigated the effect of dietary zinc deficiency during the developmental period on hepatic cytochrome P450 (CYP) expression in postpubertal male rats. Twenty-one-day-old weanling male Wistar rats were randomly assigned to one of the following dietary groups: zinc-adequate (31 mg zinc/kg diet); marginal zinc-deficient (3 mg zinc/kg diet); severe zinc-deficient (1 mg zinc/kg diet); or pair-fed control for either the marginal or severe zinc-deficient group. All rats were killed at 63 days of age. Compared with the corresponding pair-fed controls, marginal zinc deficiency decreased CYP2C11-mediated testosterone 2alpha- and 16alpha-hydroxylase activities by 43 and 42%, respectively, whereas severe zinc deficiency reduced each of these activities by approximately 60%. The decrease in CYP2C11 activity was accompanied by a reduction in CYP2C11 protein and mRNA levels, as assessed by immunoblot and reverse transcription-polymerase chain reaction (RT-PCR) assays, respectively. Additional RT-PCR analysis indicated that severe zinc deficiency decreased CYP3A2 and CYP3A18 mRNA levels by 49 and 43%, respectively, whereas it increased CYP2C12 (253%) and CYP3A9 (238%) mRNA expression. Plasma testosterone concentration was decreased by 67% in the marginal zinc-deficient group when compared with the corresponding pair-fed control group. By comparison, it was below the limit of quantification (0.2 ng/mL) in the severe zinc-deficient rats. Overall, these results indicate that dietary zinc deficiency during the developmental period feminized the hepatic gene expression of the sexually dimorphic CYP2C11, CYP3A2, CYP3A18, CYP2C12, and CYP3A9 in postpubertal male rats.
本研究调查了发育期间膳食锌缺乏对青春期后雄性大鼠肝脏细胞色素P450(CYP)表达的影响。将21日龄断乳雄性Wistar大鼠随机分为以下饮食组之一:锌充足组(31毫克锌/千克饮食);边缘性锌缺乏组(3毫克锌/千克饮食);严重锌缺乏组(1毫克锌/千克饮食);或边缘性或严重锌缺乏组的配对喂养对照组。所有大鼠在63日龄时处死。与相应的配对喂养对照组相比,边缘性锌缺乏使CYP2C11介导的睾酮2α-和16α-羟化酶活性分别降低了43%和42%,而严重锌缺乏使这些活性各自降低了约60%。CYP2C11活性的降低伴随着CYP2C11蛋白和mRNA水平的降低,分别通过免疫印迹和逆转录-聚合酶链反应(RT-PCR)分析进行评估。额外的RT-PCR分析表明,严重锌缺乏使CYP3A2和CYP3A18 mRNA水平分别降低了49%和43%,而使CYP2C12(253%)和CYP3A9(238%)mRNA表达增加。与相应的配对喂养对照组相比,边缘性锌缺乏组的血浆睾酮浓度降低了67%。相比之下,严重锌缺乏大鼠的血浆睾酮浓度低于定量下限(0.2纳克/毫升)。总体而言,这些结果表明,发育期间膳食锌缺乏使青春期后雄性大鼠肝脏中具有性别差异的CYP2C11、CYP3A2、CYP3A18、CYP2C12和CYP3A9的基因表达出现雌性化。