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三丁基锡诱导的内脏肥胖与雄性大鼠白色脂肪组织氧化还原平衡受损有关。

Tributyltin-induced visceral adiposity is associated with impaired redox balance in white adipose tissue of male rats.

机构信息

Laboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil; Research Center on Morphology and Metabolism, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.

Laboratory of Experimental Pharmacology, Department of Physiology and Pharmacology, Biomedical Institute, Fluminense Federal University, Niteroi, RJ, Brazil.

出版信息

Mol Cell Endocrinol. 2024 Nov 1;593:112343. doi: 10.1016/j.mce.2024.112343. Epub 2024 Aug 13.

Abstract

Tributyltin (TBT) is an organotin compound that has several adverse health effects, including the development of obesity. Although obesity is strongly associated with adipose redox imbalance, there is a lack of information on whether TBT promotes a pro-oxidative environment in WAT. Thus, adult male Wistar rats were randomly exposed to either vehicle (ethanol 0.4%) or TBT (1000 ng/kg) for 30 days. Body and fat pad masses, visceral fat morphology, lipid peroxidation, protein carbonylation, redox status markers, and catalase activity were evaluated. TBT promoted increased adiposity and visceral fat, with hypertrophic adipocytes, but did not alter body mass and subcutaneous fat. ROS production and lipid peroxidation were elevated in TBT group, as well as catalase protein expression and activity, although protein oxidation and glutathione peroxidase protein expression remained unchanged. In conclusion, this is the first study to demonstrate that subacute TBT administration leads to visceral adipose redox imbalance, with increased oxidative stress. This enlights the understanding of the metabolic toxic outcomes of continuous exposure to TBT in mammals.

摘要

三丁基锡(TBT)是一种有机锡化合物,具有多种不良健康影响,包括肥胖的发展。尽管肥胖与脂肪氧化还原失衡密切相关,但关于 TBT 是否会促进 WAT 中氧化环境的信息仍然缺乏。因此,成年雄性 Wistar 大鼠随机暴露于载体(0.4%乙醇)或 TBT(1000ng/kg)中 30 天。评估了体重和脂肪垫质量、内脏脂肪形态、脂质过氧化、蛋白质羰基化、氧化还原状态标志物和过氧化氢酶活性。TBT 促进了脂肪量和内脏脂肪的增加,伴有肥大的脂肪细胞,但不改变体重和皮下脂肪。TBT 组 ROS 产生和脂质过氧化增加,过氧化氢酶蛋白表达和活性增加,尽管蛋白质氧化和谷胱甘肽过氧化物酶蛋白表达保持不变。总之,这是第一项表明亚急性 TBT 给药导致内脏脂肪氧化还原失衡和氧化应激增加的研究。这阐明了对哺乳动物持续暴露于 TBT 的代谢毒性结果的理解。

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