An investigation of the effects of methylmercury in rats fed different dietary fats and proteins: Testicular steroidogenic enzymes and serum testosterone levels
An investigation of the effects of methylmercury in rats fed different dietary fats and proteins: Testicular steroidogenic enzymes and serum testosterone levels
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DOI：
10.1016/j.fct.2007.08.004
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发表时间：
2008-01-01
影响因子：
4.3
通讯作者：
Mehta, Rekha
中科院分区：
文献类型：
--
作者：
McVey, Mark J.;Cooke, Gerard M.;Mehta, Rekha
甲基汞（MeHg）是一种睾丸毒物，可导致哺乳动物和家禽的类固醇生成酶活性降低、血清睾酮（T）降低和精子发生异常。还已知某些饮食可以改变大鼠的雄激素代谢。以前，我们已经表明，在目前的研究中使用的饮食影响循环雄激素水平和睾丸类固醇生成酶的活性在Sprague道利大鼠在没有甲基汞。在本研究中，我们已经调查的影响，强加的环境污染物（甲基汞）常见于海洋哺乳动物和鱼类对大鼠的饮食摄入不同的蛋白质和脂质，以确定是否不同的饮食可以修改甲基汞毒性大鼠。因此，我们研究了甲基汞对大鼠睾丸类固醇生成酶和血清睾酮的影响，这些大鼠的饮食含有不同的蛋白质来源（酪蛋白、鱼粉、乳清）或不同的脂质来源（大豆油、二十二碳六烯酸（DHA）、鱼油、猪油）。将42-45日龄的雄性大鼠（每组18只）分配到不同的实验饮食中，持续28天，之后每组中的6只大鼠每天以0、1或3 mg/kg体重/天的氯化甲基汞溶于5 mM Na 2CO 3溶液中，持续14天，同时维持其饮食。在给药的第43天，处死大鼠，冷冻血浆和睾丸（-80 ° C，直至分析。用放射免疫法测定微粒体类固醇生成酶（3 β-HSD、17-OHase、C-17，20 - 1 yase、17 β-HSD）活性。采用ELISA试剂盒测定血清睾酮。睾丸重量不受甲基汞的影响。在所有三种蛋白质饮食中，每天3毫克/千克体重的甲基汞导致C-17，20-裂解酶活性降低（>50%），在酪蛋白和乳清蛋白喂养的大鼠中，17-OH酶活性也出现类似的降低。在3毫克/千克体重/天的剂量下，甲基汞降低了DHA饮食中的17-OHase活性，但对3 β-HSD活性没有影响，对17 β-HSD活性也没有抑制作用。甲基汞（3毫克/千克体重/天）导致乳清、大豆油和鱼油组的血清T显著降低。有趣的是，鱼粉蛋白而不是鱼油提供了一定的保护，以保持类固醇生成酶的活动和血清T水平在大鼠服用甲基汞。总之，这些研究表明，不同的脂质饮食可以改变甲基汞对雄性大鼠的血清睾酮和类固醇生成酶活性的毒性作用。皇冠版权所有（C）2007由爱思唯尔有限公司出版。保留所有权利。
Methylmercury (MeHg) is a testicular toxicant causing reduced steroidogenic enzyme activity, reduced serum testosterone (T) and abnormal spermatogenesis in mammals and fowl. It is also known that certain diets can alter androgen metabolism in rats. Previously we have shown that diets used in the current study impact circulating androgen levels and testicular steroidogenic enzyme activities in Sprague Dawley rats in the absence of MeHg. In the present study, we have investigated the impact of imposing an environmental contaminant (MeHg) commonly found in marine mammals and fish onto the rats' dietary intake of different proteins and lipids in order to determine if the different diets could modify MeHg toxicity in rats. Therefore, we examined the effects of MeHg on testicular steroidogenic enzymes and serum testosterone in rats fed diets containing either different protein sources (casein, fishmeal, whey) or different lipid sources (soybean oil, docosahexaenoic acid (DHA), sea] oil, fish oil, lard). Male rats 42-45 days of age (18 per group) were assigned to different experimental diets for 28 days after which 6 rats in each group were gavaged daily with 0, 1 or 3 mg/kg body weight (BW)/day MeHg chloride in 5 mM Na2CO3 solution for 14 days while being maintained on their diets. On the 43rd day of dosing, rats were sacrificed and blood plasma and testes frozen (-80 degrees Q until analysis. Microsomal steroidogenic enzyme activities (3 beta-HSD, 17-OHase, C-17,20-1yase, 17 beta-HSD) were measured radiometrically. Serum testosterone was determined using ELISA kits. Testis weights were not affected by MeHg. MeHg at 3 mg/kg BW/day caused a reduction (>50%) in the activity of C-17,20-lyase in all three protein diets and similar reductions in 17-OHase activity were seen in the casein and whey protein fed rats. At 3 mg/kg BW/day, MeHg reduced 17-OHase activity in the DHA diet but had no effect on 3 beta-HSD activity and no inhibitory effects on 17 beta-HSD activity. MeHg (3 mg/kg BW/day) caused significant reductions in serum T in the whey, soybean oil and fish oil groups. Interestingly, fishmeal protein but not fish oil offered some protection with respect to maintaining steroidogenic enzyme activities and serum T levels in rats dosed with MeHg. In conclusion, these studies show that different lipid diets can alter the toxic effects of MeHg on male rat steroidogenesis in terms of serum testosterone and steroidogenic enzyme activities. Crown Copyright (C) 2007 Published by Elsevier Ltd. All rights reserved.