Animals
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2019
·Vol. 10
·期 1
·74
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IF 1.832
Jiakun Shen,Aneela Perveen,Niaz Kaka,Zhaojian Li,Pengyuan Dai,Chunmei Li
Simple SummaryThis study investigated the effects of maternal T-2 toxin exposure on the development of testis in the mice offspring. The detrimental effects were assessed by testicular weight, antioxidant capacity, and testosterone synthesis and secretion. Studies have shown that the toxin carried by the mother has bad effects on the testicular development of offspring at puberty, affecting the antioxidant system and testosterone synthesis in the testis, but the maternal exposure of T-2 toxin had no significant impact on the testes of offspring after sexual maturity, suggesting the recovery of reproductive function.AbstractT-2 toxin, the most toxic member of trichothecene mycotoxin, is widely distributed in cereals, and has been extensively studied, but few studies focus on the toxicity of maternal exposure to offspring. This study focused on the effects of maternal exposure to T-2 toxin (during gestation and lactation) on the testicular development of mice offspring. Dams were orally administered with T-2 toxin at 0, 0.005, or 0.05 mg/kg body weight from the late stage of gestation to the end of lactation. Testicular samples of the mice offspring were collected on the postnatal day 21, 28, and 56. The results showed significant decreases in body weight and testicular weight on the postnatal day 28. Moreover, significant inhibition of antioxidant system and testosterone synthesis was detected on the postnatal day 28. Furthermore, there were significant decreases in the gene expression levels ofStARand3β-HSD, which are involved in testosterone synthesis. In general, present results demonstrated that maternal exposure to T-2 toxin during gestation and lactation led to bad effects on the capacity of antioxidant system and inhibited testosterone synthesis in testes during pre-puberty with no significant effects on post-puberty.Keywords:maternal exposure;oxidative stress;T-2 toxin;testicular development;testosterone synthesis
研究领域:
毒理学
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生殖生物学
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内分泌学
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PubMed
高影响因子
ANIMAL REPRODUCTION SCIENCE
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2023
·
IF 2.2
Wenjiao Liu,Ting Gong,Yongjian Xu
Testosterone is a key crucial hormone synthesized by steroidogenic enzymes that initiate and maintain spermatogenesis and secondary sexual characteristics in adult males. The taste receptor family 1 subunit 3 (T1R3) is reported to be associated with male reproduction. T1R3 can regulate the expressions of steroidogenic enzymes and affect testosterone synthesis . In this study, we addressed the question of whether the expression of steroid synthase was associated with T1R3 and its downstream-tasting molecules during testicular development . The results showed an overall upward trend in testosterone and morphological development in testes from Congjiang Xiang pigs from pre-puberty to sexual maturity. Gene expression levels of testicular steroidogenic acute regulatory protein ( StAR ), 3β-hydroxysteroid dehydrogenase ( 3β-HSD ), cytochrome P450c17 ( CYP17A1 ) and 17β-hydroxysteroid dehydrogenase ( 17β-HSD ) were increased from pre-puberty to sexual maturity. Protein expression changes of CYP17A1 and 3β-HSD were consistent with mRNA. The relative abundance of tasting molecules ( TAS1R3 , phospholipase Cβ2, PLCβ2 ) was increased from pre-puberty to puberty ( P < 0.05), with no further significant changes in expression from puberty to sexual maturity. Steroidogenic enzymes (3β-HSD and CYP17A1) were strongly detected in Leydig cells from pre-puberty to sexual maturity, while tasting molecules were localized in Leydig cells and spermatogenic cells. Correlation analysis showed that the genes mentioned above (except for PLCβ2 ) were positively correlated with testosterone levels and morphological characteristics of the testes at different developmental stages of Congjiang Xiang pigs. These results suggest that steroidogenic enzymes regulate testosterone synthesis and testicular development, and that taste receptor T1R3, but not PLCβ2, may associate with this process.
研究领域:
生殖生物学
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内分泌学
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分子生物学
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PubMed
高影响因子
Cells
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2025
·Vol. 14
·期 17
·1376
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IF 5.2
Zonghao Tang,Youkun Zheng
The maturation of testicular Leydig cells during the prepubertal stage is crucial for establishing male fertility. While diabetes is recognized as a significant detrimental factor affecting male testicular function, its impact specifically during the prepubertal period remains largely unknown. We hypothesized that prepubertal diabetes may impair testicular development by disrupting Leydig cell maturation. Using streptozotocin (STZ) administration, we established a prepubertal diabetic rat model and investigated the effects of diabetes on testicular development 2 and 4 weeks post-STZ treatment. Diabetes significantly hampered testicular development, manifesting as a decreased testicular weight, structural abnormalities, reduced testosterone levels, and increased inflammatory responses. As anticipated, prepubertal diabetes stagnated Leydig cell maturation and increased Leydig cell apoptosis. Mechanistic studies revealed that autophagy is essential for maintaining homeostasis and facilitating differentiation in immature Leydig cells but is significantly inhibited by hyperglycemia. Dysregulation of autophagy impaired the mitochondrial network, triggering inflammatory responses, suppressing steroidogenic capacity, and accumulating reactive oxygen species (ROS). Elevated ROS levels exacerbated the inflammatory response in the Leydig cells in an NLRP3-dependent manner. Inhibition of NLRP3 ameliorated the hyperglycemia-induced inflammation and decline in steroidogenic ability. Collectively, these findings demonstrate that hyperglycemia suppresses autophagy induction and enhances ROS accumulation in Leydig cells. This cascade promotes inflammation and inhibits steroidogenesis, thereby impeding testicular development in prepubertal diabetic rats.
研究领域:
内分泌学
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生殖生物学
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细胞生物学
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糖尿病研究
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高影响因子
JOURNAL OF HAZARDOUS MATERIALS
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2021
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IF 10.588
Tianxin Zhao,Xiangliang Tang,Dian Li,Jinglu Zhao,Rui Zhou,Fangpeng Shu,Wei Jia,Wen Fu,Huimin Xia,Guochang Liu
Polybrominated diphenyl ethers (PBDEs) are a widely used class of brominated flame retardants . Exposure to PBDEs could induce testicular damage in mammals, but the effects and potential mechanism of action of prenatal exposure to environmentally relevant PBDEs on testicular development remain unclear. For the in vivo study, pregnant ICR mice were exposed to environmentally relevant levels of 2,2′,4,4′,5-pentabromodiphenyl ether (PBDE-99), a major component of commercial PBDE mixtures. We found that the anogenital index and testicular organ coefficient were significantly decreased, the incidence of cryptorchidism was increased, and testicular histology was disturbed in male offspring . Transcriptomic profiling showed that steroidogenesis disorders were significant in all PBDE-99 exposure groups. The testosterone levels, expressions of testosterone regulators, and the number of CYP11A1-positive and 11β-HSD1-positive Leydig cells were significantly decreased after PBDE-99 exposure. For the in vitro study, TM3 Leydig cells were exposed to PBDE-99 at gradient concentrations. Transcriptomic profiling and validation experiments showed that PBDE-99 upregulated reactive oxygen species , activated the ERK1/2 pathway, inhibited the ubiquitination degradation pathway, and finally induced Leydig cell apoptosis. Cumulatively, these findings revealed that prenatal exposure to environmentally relevant levels of PBDE-99 leads to steroidogenesis disorders by inducing the apoptosis of Leydig cells, causing testicular dysgenesis.
研究领域:
毒理学
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生殖生物学
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环境健康
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PubMed
高影响因子
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