BIOLOGICAL TRACE ELEMENT RESEARCH
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2025
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IF 3.6
Liang Chen,Chen Mingyang,Mu Zhidan,Tian Xinyan,Zhao Wenzhen,Hu Yarong,Su Juan
The aim of this study was to explore the role of the ZnT9 protein in obesity-induced sperm maturation disorders in men. We generated a mouse model of obesity-induced weak spermatogenesis via a high-fat diet (HFD) for 10 weeks. In addition to the HFD, a 5-week intervention of salubrinal (SAL) (an inhibitor of endoplasmic reticulum stress) (1 mg/kg/day), ZnSO 4 (15 mg/kg/day), and their combination was started at week 6, after which sperm viability and epididymal tissue damage were assessed. To investigate the role of the ZnT9 protein in spermatogenesis, the expression levels of the ZnT9 protein, endoplasmic reticulum stress (ERS)–related protein, Wnt pathway protein, and apoptosis-related protein in epididymal tissue were measured. Compared with those in the normal (N) group, the mice in the HFD group presented decreased sperm motility, damaged epididymal tissue, epididymal tissue showed decreased expression of ZnT9, β-catenin, LEF protein and mRNA, and increased expression of total cholesterol (TC) and triglycerides (TG), GRP78, Caspase-3, BAX protein and mRNA, as well as increased apoptosis as shown by TUNEL staining. Compared with the HFD group, HFD + ZnSO 4 group, HFD + SAL group, and HFD + ZnSO 4 + SAL groups resulted in reduced epididymal damage, improved decreased total cholesterol (TC) and triglycerides (TG), sperm viability, increased expression of ZnT9, β-catenin, LEF protein and mRNA, and decreased expression of GRP78, Caspase-3, and BAX protein and mRNA, as well as decreased apoptosis as shown by TUNEL staining in epididymal tissues. According to this study, obesity leads to elevated ERS and affects ZnT9 protein synthesis. Inhibition of the Wnt pathway ultimately leads to cell death and damage in epididymal tissue and decreased sperm viability.
研究领域:
生殖生物学
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分子生物学
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营养学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL RESEARCH
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2020
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IF 5.715
Xuelian Zhang,Wenbo Cui,Ke Wang,Rui Chen,Mingyue Chen,Kangshu Lan,Yanpei Wei,Chuanying Pan,Xianyong Lan
Background Pesticides, especially organophosphorus pesticides such as chlorpyrifos (CPF), play an important role in modern agriculture. Studies have shown that pesticide residues are an important cause of male reproductive injury in mammal. Aim The aim of this study was to evaluate the reproductive damage caused by CPF in male mice and investigate the underlying mechanisms. Methods In vivo , C57BL/6 mice (6–8 weeks old) were treated with CPF for 14, 70, and 80 days by intraperitoneal injection, intragastric administration, and dietary supplementation, respectively. Then, sperm from the cauda epididymidis was cultured in vitro to confirm the deleterious effects of CPF. Results The in vivo results indicated that, after treatment with CPF by dietary supplementation and intraperitoneal injection, the expression of reproduction-related genes in the mouse testes was altered, although the mice were fertile and the testes presented no morphological abnormalities. Notably, mating experiments revealed that the fertility of male mice was decreased following CPF administration by gavage. Sperm motility within the cauda epididymidis declined significantly after CPF treatment, which was accompanied by a decrease in sperm density, upregulation of relative reactive oxygen species (ROS) levels, and downregulation of glutathione reductase activity. In vitro incubation experiments showed that sperm rapidly lost their capacity for linear movement; the relative ROS levels also increased significantly, while the mitochondrial membrane potential (MMP) showed a significant decrease. However, the integrity of the plasma membrane was not affected by CPF administration. Conclusions The above data indicated that exposure to CPF reduces sperm motility by disrupting mitochondrial function and increasing the level of oxidative stress during sperm maturation, thereby reducing the fecundity of male mice.
研究领域:
毒理学
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生殖生物学
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环境健康科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF PROTEOME RESEARCH
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2022
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IF 5.37
Renzheng Zhang,Xian Guo,Chunnian Liang,Jie Pei,Pengjia Bao,Mancai Yin,Fude Wu,Min Chu,Ping Yan
To achieve fertilization, mammalian spermatozoa must undergo capacitation and the acrosome reaction (AR) within the female reproductive tract. However, the effects of cryopreservation on sperm maturation and fertilizing potential have yet to be established. To gain insight into changes in protein levels within sperm cells prepared for use in the context of fertilization, a comprehensive quantitative proteomic profiling approach was used to analyze frozen–thawed Ashidan yak spermatozoa under three sequential conditions: density gradient centrifugation-based purification, incubation in a capacitation medium, and treatment with the calcium ionophore A23187 to facilitate AR induction. In total, 3280 proteins were detected in these yak sperm samples, of which 3074 were quantified, with 68 and 32 being significantly altered following sperm capacitation and AR induction. Differentially abundant capacitation-related proteins were enriched in the metabolism and PPAR signaling pathways, while differentially abundant AR-related proteins were enriched in the AMPK signaling pathway. These data confirmed a role for superoxide dismutase 1 (SOD1) as a regulator of sperm capacitation while also offering indirect evidence that heat shock protein 90 alpha (HSP90AA1) regulates the AR. Together, these findings offer a means whereby sperm fertility-related marker proteins can be effectively identified. Data are available via Proteome Xchange with identifier PXD035038.
研究领域:
生殖生物学
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蛋白质组学
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动物科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）