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大鼠母体肥胖会损害雄性后代睾丸抗氧化防御系统的衰老。

Maternal obesity in the rat impairs male offspring aging of the testicular antioxidant defence system.

作者信息

Bautista Claudia J, Rodríguez-González Guadalupe L, Morales Angélica, Lomas-Soria Consuelo, Cruz-Pérez Fabiola, Reyes-Castro Luis A, Zambrano Elena

机构信息

Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Departamento de Biología de la Reproducción, Vasco de Quiroga 15, Belisario Domínguez, Tlalpan, 14080, México, D.F. México.

出版信息

Reprod Fertil Dev. 2017 Sep;29(10):1950-1957. doi: 10.1071/RD16277.

Abstract

A high-fat diet during intrauterine development predisposes offspring (F) to phenotypic alterations, such as lipid synthesis imbalance and increased oxidative stress, causing changes in male fertility. The objective of this study was to evaluate the effects of maternal obesity during pregnancy and lactation on antioxidant enzymes in the F testes. Female Wistar rats (F) were fed either a control (C, 5% fat) or an obesogenic (MO, maternal obesity, 25% fat) diet from weaning and throughout subsequent pregnancy and lactation. F offspring were weaned to the control diet. Testes were retrieved at 110, 450 and 650 postnatal days (PND) for real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and immunohistochemical (IHC) antioxidant enzyme analyses. Catalase was similar between groups by RT-qPCR, whereas by IHC it was higher in the MO group at all ages than in the C group. Superoxide dismutase 1 (SOD1) had lower expression at PND 110 in MO than in C by both techniques; at PND 450 and 650 by immunoanalysis SOD1 was higher in MO than in C. Glutathione peroxidase 1 (GPX1), GPX2 and GPX4 by RT-qPCR were similar between groups and ages; by IHC GPX1/2 was higher in MO than in C, whereas GPX4 showed the opposite result at PND 110 and 450. In conclusion, antioxidant enzymes in the rat testes are modified with age. Maternal obesity negatively affects the F testicular antioxidant defence system, which, in turn, can explain the decrease in reproductive capacity.

摘要

宫内发育期间的高脂饮食会使后代(F)易出现表型改变,如脂质合成失衡和氧化应激增加,从而导致雄性生育能力发生变化。本研究的目的是评估孕期和哺乳期母体肥胖对F代睾丸中抗氧化酶的影响。雌性Wistar大鼠(F)从断奶后直至随后的整个孕期和哺乳期,分别喂食对照饮食(C,5%脂肪)或致肥胖饮食(MO,母体肥胖,25%脂肪)。F代后代断奶后改为对照饮食。在出生后第110、450和650天(PND)取出睾丸,进行实时定量逆转录聚合酶链反应(RT-qPCR)和免疫组织化学(IHC)抗氧化酶分析。通过RT-qPCR检测,过氧化氢酶在各组间相似,但通过IHC检测,MO组在所有年龄段的过氧化氢酶水平均高于C组。两种技术检测均显示,在PND 110时,MO组超氧化物歧化酶1(SOD1)的表达低于C组;在PND 450和650时,免疫分析显示MO组SOD1的表达高于C组。通过RT-qPCR检测,谷胱甘肽过氧化物酶1(GPX1)、GPX2和GPX4在各组和各年龄段间相似;通过IHC检测,MO组GPX1/2高于C组,而在PND 110和450时,GPX4的结果则相反。总之,大鼠睾丸中的抗氧化酶会随年龄而发生改变。母体肥胖会对F代睾丸的抗氧化防御系统产生负面影响,进而可以解释生殖能力的下降。

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