How Does Maternal Lipopolysaccharide Exposure Impact Prenatal Testicular Development in Rats, and Could α-Tocopherol Provide a Protective Effect? A Histological, Immunohistochemical and Biochemical Study

IF 1.6 4区医学 Q4 DEVELOPMENTAL BIOLOGY

Birth Defects Research Pub Date : 2025-05-02 DOI:10.1002/bdr2.2469

Shimaa Antar Fareed, Heba El-Sayed Mostafa, Yousif Mohamed Saleh, Yasmin Islam Magdi, Islam Mohamed Magdi Ammar

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Abstract

Background

Lipopolysaccharides or endotoxins trigger proinflammatory cytokines and nitric oxide release, whereas α-tocopherol protects cells from oxidative damage. This study investigated the effects of maternal lipopolysaccharide exposure on prenatal testicular development in male rat offspring and assessed α-tocopherol's protective role.

Methods

Forty pregnant female rats were divided into four groups. Group I (control) included a negative control receiving normal saline and a positive control receiving 30 mg/kg of α-tocopherol intraperitoneally from the 3rd to 18th gestational day. Group II received 50 mg/kg of lipopolysaccharides intraperitoneally from the 13th to 17th gestational day, whereas Group III received both α-tocopherol and lipopolysaccharides at the same dosages. On the seventh day postpartum, fetuses were weighed, sexed, and dissected; sera from male fetuses were collected for biochemical analysis, and fetal testes were used for histology, immunohistochemistry, and morphometry.

Results

Rats treated with lipopolysaccharide showed reduced body weight, testosterone, and luteinizing hormone levels, with histopathological changes, including thickened testicular capsules and abnormalities in the number, size, shape, and cellular components of seminiferous tubules. These adverse effects were improved by α-tocopherol supplementation.

Conclusion

We concluded that lipopolysaccharide exposure during pregnancy impairs testicular development and steroidogenesis, which are ameliorated by α-tocopherol coadministration.

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母体脂多糖暴露如何影响大鼠产前睾丸发育，α-生育酚是否有保护作用？A组织、免疫组织化学和生化研究

脂多糖或内毒素可触发促炎细胞因子和一氧化氮的释放，而α-生育酚可保护细胞免受氧化损伤。本研究探讨了母体脂多糖暴露对雄性大鼠子代产前睾丸发育的影响，并评估了α-生育酚的保护作用。方法40只妊娠雌性大鼠分为4组。ⅰ组（对照组）为阴性对照组，从妊娠第3 ~ 18天开始腹腔注射生理盐水，阳性对照组注射30 mg/kg α-生育酚。II组在妊娠第13 ~ 17天腹腔注射50 mg/kg脂多糖，III组同时注射相同剂量的α-生育酚和脂多糖。产后第7天，对胎儿进行称重、性别鉴定和解剖；采集男性胎儿血清进行生化分析，对胎儿睾丸进行组织学、免疫组织化学和形态计量学分析。结果脂多糖组大鼠体重减轻，睾酮和黄体生成素水平降低，组织病理改变，包括睾丸囊增厚，精小管数量、大小、形状和细胞成分异常。补充α-生育酚可改善这些不良反应。结论妊娠期脂多糖暴露会影响睾丸发育和类固醇生成，而α-生育酚可改善这一影响。

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来源期刊

Birth Defects Research Medicine-Embryology

CiteScore

3.60

自引率

9.50%

发文量

153

期刊介绍： The journal Birth Defects Research publishes original research and reviews in areas related to the etiology of adverse developmental and reproductive outcome. In particular the journal is devoted to the publication of original scientific research that contributes to the understanding of the biology of embryonic development and the prenatal causative factors and mechanisms leading to adverse pregnancy outcomes, namely structural and functional birth defects, pregnancy loss, postnatal functional defects in the human population, and to the identification of prenatal factors and biological mechanisms that reduce these risks. Adverse reproductive and developmental outcomes may have genetic, environmental, nutritional or epigenetic causes. Accordingly, the journal Birth Defects Research takes an integrated, multidisciplinary approach in its organization and publication strategy. The journal Birth Defects Research contains separate sections for clinical and molecular teratology, developmental and reproductive toxicology, and reviews in developmental biology to acknowledge and accommodate the integrative nature of research in this field. Each section has a dedicated editor who is a leader in his/her field and who has full editorial authority in his/her area.