EFFECTS OF DIETARY ALPHA-TOCOPHEROL AND BETA-CAROTENE ON LIPID-PEROXIDATION INDUCED BY METHYL MERCURIC-CHLORIDE IN MICE
EFFECTS OF DIETARY ALPHA-TOCOPHEROL AND BETA-CAROTENE ON LIPID-PEROXIDATION INDUCED BY METHYL MERCURIC-CHLORIDE IN MICE
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DOI：
10.1111/j.1600-0773.1993.tb01563.x
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发表时间：
1993-10-01
期刊：
影响因子：
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通讯作者：
ANDERSEN, O
中科院分区：
文献类型：
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作者：
ANDERSEN, HR;ANDERSEN, O
雄性CBA小鼠暴露于氯化甲基汞（CH 3 HgCl，10-40毫克/升的饮用水）2周，导致剂量相关的汞沉积和肝，肾和脑脂质过氧化作用增强。给小鼠喂食含有不同水平的α-生育酚（10、100或1000 mg/kg）或β-胡萝卜素（1000、10000或100000 IU/kg）的定义明确的半合成饮食四周，每种饮食两组。使用的α-生育酚和β-胡萝卜素浓度分别对应于缺乏、正常和高水平。在最后两周内，每种饮食的一组给予40 mg CH 3 HgCl/l饮用水。高饮食α-生育酚保护对CH 3 HgCl诱导的肝脂质过氧化，而α-生育酚缺乏饮食进一步增强CH 3 HgCl诱导的肝脂质过氧化。类似地，虽然在肾脏中发生了统计学上不显著的影响，但α-生育酚并不能防止CH 3 HgCl诱导的大脑脂质过氧化。过量膳食β-胡萝卜素进一步增强CH_3HgCl诱导的肝、肾和脑脂质过氧化作用。CH_3HgCl显著降低了各饲料组大鼠肾脏中总谷胱甘肽过氧化物酶（T-GSH-Px）和硒依赖型谷胱甘肽过氧化物酶（Se-GSH-Px）的活性。与喂食正常水平α-生育酚的小鼠相比，高膳食α-生育酚增强了肝脏和肾脏中Se-GSH-Px的活性。这发生在暴露于CH_3-HgCl的小鼠和未暴露的小鼠中，并且暴露于CH_3-HgCl的小鼠和未暴露的小鼠之间的差异没有减小。高α-生育酚可增加CH_3HgCl染毒小鼠脑中Se-GSH-Px和T-GSH-Px的活性。膳食中β-胡萝卜素的水平并不影响这两种酶的活性的器官调查。
Exposure of male CBA mice to methyl mercuric chloride, CH3HgCl, (10-40 mg/1 in drinking water) for 2 weeks resulted in dose-related Hg deposition and enhanced lipid peroxidation in liver, kidney and brain. Mice were fed well-defined semisynthetic diets containing different levels of alpha-tocopherol (10, 100 or 1000 mg/kg) or beta-carotene (1000, 10000 or 100000 IU/kg) for four weeks, two groups on each diet. The concentrations of alpha-tocopherol and beta-carotene used corresponded to deficient, normal and high levels. During the last two weeks, one group on each diet was given 40 mg CH3HgCl/l of drinking water. High dietary alpha-tocopherol protected against CH3HgCl induced hepatic lipid peroxidation, whereas the alpha-tocopherol deficient diet further enhanced CH3HgCl induced hepatic lipid peroxidation. Similar, though statistically non-significant effects occured in the kidneys, alpha-Tocopherol did not protect against CH3HgCl induced lipid peroxidation in the brain. Excess dietary beta-carotene further enhanced CH3HgCl induced lipid peroxidation in liver, kidney and brain. CH3HgCl significantly decreased the activity of total glutathione peroxidase (T-GSH-Px) and Se-dependent glutathione peroxidase (Se-GSH-Px) in the kidneys in all dietary groups. High dietary alpha(-tocopherol enhanced the activity of Se-GSH-Px in liver and kidney compared to the activity in mice fed the normal level of alpha-tocopherol. This occured in mice exposed to CH3-HgCl as well as in unexposed mice, and the difference between CH3HgCl exposed and unexposed mice was not diminished. High dietary a-tocopherol increased the activity of both Se-GSH-Px and T-GSH-Px in the brain of CH3HgCl-exposed mice. The dietary level of beta-carotene did not affect the activity of the two enzymes in the organs investigated.