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膳食低聚果糖可降低甲基汞暴露小鼠大脑中的汞含量。

Dietary Fructooligosaccharides Reduce Mercury Levels in the Brain of Mice Exposed to Methylmercury.

机构信息

Department of Basic Medical Sciences, National Institute for Minamata Disease.

Department of Environment and Public Health, National Institute for Minamata Disease.

出版信息

Biol Pharm Bull. 2021;44(4):522-527. doi: 10.1248/bpb.b20-00806.

Abstract

Methylmercury (MeHg) exposure during pregnancy is a concern because of its potential health risks to fetuses. Intestinal microbiota has important roles in the decomposition and fecal excretion of MeHg. We investigated the effect of nondigestible saccharides on the accumulation and excretion of Hg after MeHg exposure. Female BALB/cByJ mice were fed a basal diet or the same diet supplemented with 5% fructooligosaccharides (FOS) or 2.5% glucomannan. Six weeks after feeding, mice were administered MeHg chloride (4 mg Hg/kg, per os (p.o.)), and urine and feces were collected for 28 d. FOS-fed mice had lower total Hg levels in all tissues (including the brain) compared with that of controls. The glucomannan diet had no effect on tissue Hg levels. No differences in tissue concentrations of inorganic Hg among groups were found. Fecal Hg excretion was markedly higher in FOS-fed mice than that in controls, but urinary Hg excretion was similar. FOS-fed mice had a higher proportion of inorganic Hg in feces than that of controls, with a significant increase in fecal Hg excretion. Analysis of fecal bacterial population showed the relative abundance of Bacteroides in FOS-fed mice to be higher than that in controls. The results suggest that FOS enhanced fecal Hg excretion and decreased tissue Hg levels after MeHg administration, possibly by accelerating MeHg demethylation by intestinal bacteria (the candidate genus Bacteroides). This demethylation also reduces MeHg absorption in the large intestine. In conclusion, daily FOS intake may decrease tissue Hg levels in animals and humans exposed to MeHg.

摘要

孕期甲基汞(MeHg)暴露令人担忧,因为其对胎儿存在潜在健康风险。肠道微生物群在 MeHg 的分解和粪便排泄中具有重要作用。我们研究了不可消化的糖对 MeHg 暴露后汞积累和排泄的影响。雌性 BALB/cByJ 小鼠喂食基础饮食或相同饮食,添加 5%低聚果糖(FOS)或 2.5%葡甘露聚糖。喂养 6 周后,经口给予小鼠 MeHg 氯化物(4mgHg/kg),并收集尿液和粪便 28 天。与对照组相比,FOS 喂养的小鼠所有组织(包括大脑)中的总汞水平均较低。葡甘露聚糖饮食对组织汞水平没有影响。各组间组织中无机汞浓度无差异。FOS 喂养的小鼠粪便中汞排泄量明显高于对照组,但尿液中汞排泄量相似。FOS 喂养的小鼠粪便中无机汞比例高于对照组,粪便中汞排泄量显著增加。粪便细菌种群分析显示,FOS 喂养的小鼠中拟杆菌的相对丰度高于对照组。结果表明,FOS 增强了 MeHg 给药后粪便中汞的排泄,降低了组织中的汞水平,这可能是通过加速肠道细菌(候选属拟杆菌)的 MeHg 脱甲基作用实现的。这种脱甲基作用还减少了大肠对 MeHg 的吸收。总之,每日摄入 FOS 可能会降低接触 MeHg 的动物和人类的组织汞水平。

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