BPA Exacerbates Zinc Deficiency-Induced Testicular Tissue Inflammation in Male Mice Through the TNF-α/NF-κB/Caspase8 Signaling Pathway.

IF 3.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Biological Trace Element Research Pub Date : 2025-08-01 Epub Date: 2024-12-06 DOI:10.1007/s12011-024-04464-2
Xinying Wang, Jing Ma, Wen Li, Zhan Hou, Huanhuan Li, Yuanjing Li, Shusong Wang, Yanqing Tie
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Abstract

Bisphenol A (BPA) is an endocrine-disrupting chemical that is toxic to reproduction. Zinc (Zn) plays an important role in male reproductive health. Zn deficiency (ZD) can co-exist with BPA. In order to investigate the specific mechanism of reproductive damage caused by BPA exposure in ZD male mice, a mouse model of ZD, BPA exposure, and their combined exposure was established in this study. Forty 4-week-old SPF male ICR mice with an average body weight of 31.7 ± 4.2 g were divided into four groups including normal Zn diet group 30 mg/(kg•d), BPA exposure group 150 mg/(kg•d), zinc deficiency diet group 7.5 mg/(kg•d), and BPA + ZD combined exposure group (BPA 150 mg/(kg•d) + ZD 7.5 mg/(kg•d)). The mice were kept for 8 weeks. The results showed that the testicular tissue structure was disturbed, and semen quality, serum Zn, testicular tissue Zn, and testicular tissue free Zn ions were decreased in the BPA-exposed and ZD groups. The expression of zinc transporters (ZIP7, ZIP8, ZIP13, and ZIP14) in testicular tissue was changed. The expressions of pro-inflammatory cytokines including TNF-α and IL-1β as well as inflammatory pathway-related proteins (IKB-α, p-IKB-α, NF-κB, p-NF-κB, Caspase8, and Caspase3) were increased, while the expressions of anti-inflammatory cytokines (TGF-β and IL-10) were decreased. The changes in the above indexes in the BPA + ZD group were more obvious. Both BPA exposure and ZD can induce testicular tissue inflammation through the TNF-α/NF-κB/Caspase8 signaling pathway, and BPA further aggravates zinc deficiency-induced testicular tissue inflammation and apoptosis damage.

BPA通过TNF-α/NF-κB/Caspase8信号通路加重锌缺乏引起的雄性小鼠睾丸组织炎症
双酚A (BPA)是一种干扰内分泌的化学物质,对生殖有害。锌(Zn)在男性生殖健康中起着重要作用。锌缺乏症(ZD)可与BPA共存。为了探讨BPA暴露对ZD雄性小鼠生殖损伤的具体机制,本研究建立了ZD、BPA暴露及其联合暴露小鼠模型。选取40只平均体重为31.7±4.2 g的4周龄SPF级雄性ICR小鼠,分为正常锌饲粮组(30 mg/(kg•d))、BPA暴露组(150 mg/(kg•d))、缺锌饲粮组(7.5 mg/(kg•d))和BPA + ZD联合暴露组(BPA 150 mg/(kg•d) + ZD 7.5 mg/(kg•d)) 4组。小鼠饲养8周。结果表明:bpa暴露组和ZD暴露组大鼠睾丸组织结构受到干扰,精液质量、血清锌、睾丸组织锌和睾丸组织游离锌离子均降低;锌转运蛋白ZIP7、ZIP8、ZIP13、ZIP14在睾丸组织中的表达发生改变。促炎因子TNF-α、IL-1β表达升高,炎症通路相关蛋白IKB-α、p-IKB-α、NF-κB、p-NF-κB、Caspase8、Caspase3表达升高,抗炎因子TGF-β、IL-10表达降低。BPA + ZD组以上指标变化更为明显。BPA暴露和ZD均可通过TNF-α/NF-κB/Caspase8信号通路诱导睾丸组织炎症,BPA进一步加重锌缺乏诱导的睾丸组织炎症和细胞凋亡损伤。
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来源期刊
Biological Trace Element Research
Biological Trace Element Research 生物-内分泌学与代谢
CiteScore
8.70
自引率
10.30%
发文量
459
审稿时长
2 months
期刊介绍: Biological Trace Element Research provides a much-needed central forum for the emergent, interdisciplinary field of research on the biological, environmental, and biomedical roles of trace elements. Rather than confine itself to biochemistry, the journal emphasizes the integrative aspects of trace metal research in all appropriate fields, publishing human and animal nutritional studies devoted to the fundamental chemistry and biochemistry at issue as well as to the elucidation of the relevant aspects of preventive medicine, epidemiology, clinical chemistry, agriculture, endocrinology, animal science, pharmacology, microbiology, toxicology, virology, marine biology, sensory physiology, developmental biology, and related fields.
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