Journal of Ocean University of China
·
2015
·Vol. 14
·期 4
·695-702
·
IF 0.558
Xu Houguo,Huang Lina,Liang Mengqing,Zheng Keke,Wang Xinxing
A 3-month feeding experiment was conducted in an in-door seawater system to investigate the effect of dietary vitamin E (Ve) on the sperm quality of turbot ( Scophthalmus maximus ). D-α-tocopherol acetate was supplemented to the basal (control) diet (65.14 mg kg −1 Ve) to obtain low and high levels of dietary Ve (244.60 mg kg −1 , LVe; 721.60 mg kg −1 , HVe). Compared with the control, sperm concentration was significantly increased in Ve-supplemented groups (LVe and HVe); while relative sperm volume and testis-somatic index were significantly increased in group HVe only. Sperm motility duration was significantly longer in group HVe than in the control, but no significant difference was observed in percent motility among groups. Sperm size, the uniformity of mitochondrial size, and the integrity of mitochondria cristae and plasma membrane were improved by dietary Ve, especially in HVe. The content of Ve in testis and liver as well as polyunsaturated fatty acids in sperm increased with dietary Ve. These results suggested that dietary Ve, especially at the high level (721.60 mg kg −1 ), significantly improved sperm concentration and motility duration and maintained normal sperm morphology of turbot.
研究领域:
水产养殖学
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营养学
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生殖生物学
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DOI
高影响因子
ENVIRONMENTAL RESEARCH
·
2025
·
IF 7.7
Zhenjun Zhao,Jingyi Chi,Zhang FangFang,Yinglin Song,Wenda Xv,Yan Li,Hui Shi
4-Octylphenol, a major environmental degradation product of alkylphenols (Aps) used in industry, is an endocrine-disrupting chemical with significant estrogenic activity. It is one of the most toxic Aps, poorly biodegradable in the environment, and can accumulate in organisms through the food chain, thereby affecting the male reproductive system. In this study, the effect of 4-octylphenol on male reproductive health was analyzed. Male pubertal mice were exposed to 4-octylphenol at doses of 0, 1, 10, and 100 mg/kg once daily for 28 days. Our findings indicated that pubertal exposure to 4-octylphenol has significant negative effects on the male reproductive system. Pubertal mice exposed to 4-octylphenol exhibited dose-dependent reproductive toxicity. In the medium- and high-dose groups, a significant reduction in testicular mass, structural damage to the seminiferous tubules, increased oxidative stress and apoptosis within the testicular tissue, and a decline in sperm quality were observed. Additionally, autophagy processes in the testicular tissue, germ cell proliferation, and meiotic processes are inhibited. Serum testosterone and estradiol levels decreased, whereas oxidative stress levels in the testes and spermatozoa increased. In contrast, the low-dose group showed only a reduction in body weight, a decrease in motile sperm count, and mild oxidative stress in the testes without significant pathological changes in Western blot experiments. These results indicate that 4-octylphenol exposure during puberty caused reproductive toxicity in male mice.
研究领域:
毒理学
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内分泌学
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生殖健康
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产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2025
·
IF 2.2
Siyu Yuan,Jun Guo,Bijun Yang,Aolin Xiao Huang,Shuqi Hu,Yingcan Li,Jingxuan Chen,Bin Yuan,Jing Yang
Cadmium (Cd) is a prevalent contaminant in both dietary and drinking water sources, posing harm to multiple tissues and disrupting reproductive function. Recent evidence indicates that natural products derived from plants may offer a mitigating Cd-induced tissue damage. However, the protective role of Liquiritigenin (LQ) and its underlying mechanism remain unclear. The present study was to investigate the protective effect of LQ against short-term, low-dose Cd-induced multi-organ damage. Notably, Cd exposure had no significant impact on body or tissue weight but did induce damage to the heart, liver, lungs, kidneys and testes of mice, while also reducing sperm quality. These adverse effects were reversed by LQ treatment, suggesting that LQ alleviates Cd toxicity. Mechanistically, LQ inhibited testicular apoptosis by modulating the protein levels of Bad, Caspase-3, Bax, Bcl-2, and NF-κB. Furthermore, molecular docking and molecular dynamics simulations provided insights into the interaction between LQ and the androgen receptor (AR). Further studies indicate that LQ increases AR level and further prevent testicular damage. Collectively, these findings support the potential of LQ in preventing Cd-induced tissue damage, particularly in the context of reproductive toxicity.
研究领域:
毒理学
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生殖生物学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOLOGICAL TRACE ELEMENT RESEARCH
·
2023
·Vol. 202
·期 7
·3180-3192
·
IF 3.9
Nong Weihua,Wei Gaomeng,Wang Junli,Lei Xiaocan,Wang Jinyuan,Wei Yanhong,Dong Mingyou,He Liqiao
This study aimed to investigate the protective effect of nicotinamide mononucleotide (NMN) on testicular spermatogenesis in aluminum chloride (AlCl 3 )-exposed rats and to elucidate the potential underlying mechanism. The results indicated that AlCl 3 -induced testicular damage, leading to reduced sperm quality, increased apoptosis, decreased cell proliferation, and impaired Sertoli cell function in rats. Additionally, glycolytic metabolism was observed to be hindered. However, after NMN treatment, there was a noticeable improvement in testicular damage among the rats, marked by increased sperm quality, reduced apoptosis, enhanced cell proliferation, improved Sertoli cell function, and an activated glycolytic metabolism. The findings of this study suggest that NMN alleviates testicular spermatogenesis impairment induced by AlCl 3 exposure through the inhibition of spermatogenic cell apoptosis, promotion of spermatogenic cell proliferation, and activation of glycolytic pathways. The study contributes an experimental foundation for potential future clinical applications of NMN in cases of AlCl 3 -exposed spermatogenic dysfunction.
研究领域:
生殖生物学
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毒理学
·
代谢生物学
✓ 已验证
DOI
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2025
·
IF 6.1
Mei-Ling Le,Yi-Qi Wan,Jia-Yu Xue,Shi-Yi Deng,Bin-Hui Wang,Li-Hai Wu,Hou-Peng Wang,Yang-Yang Yuan,Xiao-Dong Kuang,Tao Luo,Da-Lei Zhang
Hexafluoropropylene oxide (HFPO) homologues (HFPOs), presenting HFPO-dimeric acid (DA), HFPO-trimeric acid (TA) and HFPO-tetrameric acid (TeA), are emerging replacements for legacy perfluorooctanoic acid that are increasingly used for a variety of industrial applications. These novel fluorinated compounds have attracted much attention due to their environmental ubiquity and potential toxicities. However, there is a lack of clarity about their toxicological impact on male reproductive health. In our study, the mouse model was used to investigate the toxic effects of HFPOs on male reproductive function and their underlying mechanisms. The results revealed that male mice exposed to HFPOs for 8 weeks presented structural and functional abnormalities in the testis and mature sperm, as evidenced by destructed seminiferous tubule, decreased testosterone levels and sperm quality. Furthermore, treatment with HFPOs elevated reactive oxygen species and malondialdehyde content and diminished superoxide dismutase activity and succinate dehydrogenase levels, along with downregulated anti-apoptotic BCL-2 expression and upregulated pro-apoptotic BAX expression. Moreover, oral administration of HFPOs impaired testicular mitochondrial structure along with reduction in ATP content and mitochondrial DNA copy number and disruption of mitochondrial dynamics. In summary, HFPOs can impair male fertility by disrupting spermatogenesis and reducing sperm quality through multiple mechanisms, including mitochondrial dysfunction-induced oxidative stress, apoptosis, and suppression of steroidogenesis. This work aims to improve our comprehension regarding the potential risks and adverse impacts of exposure to HFPO congeners on male reproductive health.
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
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产品关联
DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
·
2024
·
IF 3.9
Xin Gao,Huan He,Qi Zheng,Siju Chen,Yu Wei,Taifa Zhang,Yi Wang,Bo Wang,Dake Huang,Shengquan Zhang,Sumei Zhang,Jinxia Zhai
BDE-209 exposure induced male reproductive toxicity with sperm quality decline. However, the role of autophagy in this was unclear. The purpose was to evaluate the protective effect and its potential mechanism of trehalose (Tre, autophagy inducer) on reproductive damage during spermiogenesis induced by BDE-209. We used 2% w/v Tre and 75 mg/kg/d BDE-209 cotreated mice for 42 days. GC-2 spd cells were cotreated with Tre, chloroquine (CQ, inhibition of autophagic flux), compound C (CC, AMPK inhibitor), and BDE-209. Tre intake significantly recovered decrease in sexual organ ratio and poor sperm quality in BDE-209-exposed mice. Supplementation with Tre rescued sperm head malformation by improving aberrant histone-protamine exchange in BDE-209-exposed mice. However, Tre intake couldn't restore the acrosome biogenesis. In addition, Tre supplementation improved testicular damage induced by BDE-209. BDE-209 blocked autophagic flux with increased P62 and LC3BⅡ/Ⅰ levels. Mechanistically, CQ treatment aggravated elevation of P62 and LC3BⅡ/Ⅰ levels induced by BDE-209, otherwise, CC and Tre treatments inhibited the rise in p-AMPK, p-ULK1, P62 and LC3BⅡ/Ⅰ levels induced by BDE-209. Tre supplementation improved reproductive injury in BDE-209-exposed mice by regulating autophagic flow via AMPK-ULK1 signaling pathways, which providing a new theoretical basis and possible therapeutic targets for male reproductive toxicity.
研究领域:
生殖毒理学
·
分子生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2024
·
IF 7.6
Dajun Gao,Caoxu Zhang,Huaqi Guo,Huan Xu,Hui Liu,Zhong Wang,Bin Xu,Wei Gang
The harmful effects of microplastics (MPs) on male fertility are receiving more and more attention. However, the impact of low-dose MPs exposure on the reproductive function of male mice is still unclear. In this study, we exposed male mice to low-dose MPs (25–30 μg/kg body weight/day) or low-dose MPs combined with high-fat diet (HFD) feeding. Our results showed that low-dose MPs exposure or HFD feeding significantly reduced sperm quality and the number of offspring born, while low-dose MPs exposure combined with HFD feeding further enhanced the above effects. The combination of low-dose MPs exposure and HFD feeding resulted in a notable elevation of inflammatory level within the prostate of mice and induced apoptosis of prostate epithelium and a decrease in nutrients (zinc, citrate) in seminal plasma fluid. Our findings in this study could provide valuable clues for better understanding the influence of low-dose MPs exposure on the reproductive system under metabolic disorders and facilitate the development of the prevention of reproductive toxicity caused by MPs exposure.
CAS / MDL:
研究领域:
环境科学
·
生殖生物学
·
毒理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2021
·
IF 6.291
Helin Chen,Yanyan Wang,Jie Luo,Min Kang,Jin Hou,Ruoping Tang,Ling Zhao,Fei Shi,Gang Ye,Xiaoli He,Hengmin Cui,Hongrui Guo,Yinglun Li,Huaqiao Tang
Nano-copper has been increasingly employed in various products. In previous studies, we showed that nano-copper caused damage in the rat testis, but it remains unclear whether the toxic reaction can affect the reproductive function. In this study, following 28 d of exposure to nano-copper at a dose of 44, 88, and 175 mg/kg/day, there was a decrease in sperm quality, fructose content, and the secretion of sex hormones. Nano-copper also increased the level of oxidative stress, sperm malformation rate, and induced abnormal structural changes in testicular tissue. Moreover, Nano-copper upregulated the expression of apoptosis-related protein Bax and autophagy-related protein Beclin, and downregulated the expression of Bcl2 and p62. Furthermore, nano-copper (175 mg/kg) downregulated the protein expression of AMPK, p-AKT, mTOR, p-mTOR, p-4E-BP1, p70S6K, and p-p70S6K, and upregulated the protein expression of p-AMPK. Therefore, nano-copper induced damage in testicular tissues and spermatogenesis is highly related to cell apoptosis and autophagy by regulating the Akt/mTOR signaling pathway. In summary, excess exposure to nano-copper may induce testicular apoptosis and autophagy through AKT/mTOR signaling pathways, and damage the reproductive system in adult males, which is associated with oxidative stress in the testes.
研究领域:
毒理学
·
生殖生物学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ENVIRONMENT INTERNATIONAL
·
2022
·
IF 13.352
Lixiao Zhou,Ziying Yu,Yinyin Xia,Shuqun Cheng,Jieying Gao,Wei Sun,Xuejun Jiang,Jun Zhang,Lejiao Mao,Xia Qin,Zhen Zou,Jingfu Qiu,Chengzhi Chen
As a new widespread contaminant, nanoplastics (NPs) pose a potential risk to human health. Nevertheless, the adverse effects of NPs on the male reproductive system are poorly understood. In this study, we aimed to determine the effects of polystyrene nanoplastics (PS-NPs) (50 nm) on sperm quality, with a focus on the acrosome defects. After 35 days of intragastric administration, sperm quality was decreased and testicular structures were impaired in mice exposed to PS-NPs in both the medium (1.0 mg/kg) and high dose (10 mg/kg) groups. No significant changes were observed in the low dose (0.2 mg/kg) group. Meanwhile, acrosome parameters including acrosome integrity and acrosome reaction were decreased after the administration of PS-NPs. These findings were consistent with the disruption of acrosome biogenesis, as identified by the changed testicular ultrastructure. Additionally, the findings were further validated using seven marker genes ( Gba2, Pick1, Gopc, Hrb, Zpbp1, Spaca1 and Dpy19l2 ) essential for acrosome formation, which showed that two of these genes ( Gopc and Dpy19l2 ) were significantly down-regulated. Moreover, repressed autophagy was observed in the testes of PS-NPs-exposed mice based on autophagy-related protein expression. This phenomenon was further verified in GC-2spd cells treated with PS-NPs (50 μg/mL, 100 μg/mL, 200 μg/mL for 24 h). The potential role of autophagy in such acrosome defects was explored by using the autophagy inhibitor 3-methyladenine (3-MA), autophagy activator rapamycin or beclin-1 siRNA. The results showed that Golgi-associated vesicle disorganization was exacerbated with the 3-MA and beclin-1 siRNA pretreatments, but decreased with the rapamycin pretreatment, and the expression of GOPC and DPY19L2 was also altered. These results indicated that autophagy might be involved in the PS-NPs-induced acrosome lesions based on the regulation of two key acrosome-formation proteins, GOPC and DPY19L2. Altogether, our results will provide new insights into the PS-NPs-induced male reproductive impairment.
研究领域:
毒理学
·
生殖生物学
·
纳米技术
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2024
·
IF 6.2
Danni Jiang,Yang Yang,Xiaojuan Han,Qianni Li,Pengfei Li,Yang Xu,Lan Chao
Past studies have observed that BHPF induces multi-organ toxicity, however, whether it induces damage to male reproductive system and the specific mechanism remains unclear. In the present study, male mice were given 0, 2, 10 or 50 mg/kg/day of BHPF by gavage for 35 days to observe its effect on reproductive organ and sperm quality. The results indicated that BHPF decreased sperm count and sperm motility in a dose-dependent manner. Besides, our results demonstrated that BHPF triggered the proliferation inhibition and cell death of germ cells in vivo and in vitro. Also, BHPF reduced the expression of function markers for germ cells, Sertoli cells, and Leydig cells, indicating its damage to function of testis cells. Simultaneously, testicular microenvironment was found to be altered by BHPF, as presented with declined testosterone level and decreased expression of local microenvironment regulators. Overall, our findings indicated the detrimental effects of BHPF on male reproductive function in mice, suggesting testicular function and local microenvironment disturbance as mechanism underlying testicular damage.
研究领域:
毒理学
·
生殖生物学
·
内分泌学
✓ 已验证
DOI
高影响因子
Frontiers in Endocrinology
·
2025
·
IF 4.6
Emmanuel Osei Nkansah,Yunzhu Lan,Hui Zhang,Binbin Xu,Qiaodan Li,Mohammad Ishraq Zafar,Jian Xu
Background: Obesity is associated with hormonal imbalance, increased oxidative stress, and inflammation in the testis. These conditions adversely affect sperm quality, leading to impaired male fertility. Therefore, therapeutic interventions to counteract the adverse effects of obesity are crucial. This study explored the therapeutic effects of 4-hydroxyisoleucine (4-HIL) on fertility in male mice with diet-induced obesity.Methods: C57BL6 male mice (n=45) were randomly divided into normal diet (ND, n=15) and high-fat diet (HFD, n=30) groups for 10 weeks. The HFD group was then randomized into untreated (HFD, n=15) and 4-HIL-treated (200 mg/kg/day, intraperitoneal injection, HFD + 4-HIL group, n=15) for 6 weeks. ND and HFD controls received saline (0.3 mL/30 g body weight) throughout the intervention period. Comprehensive evaluations included (1) metabolic assessments (body weight, glucose, insulin and pyruvate tolerance tests, and blood serum lipids), (2) sperm analysis (count, concentration, and morphology), (3) fertility testing (mating trials and in vitro fertilization), (4) testicular histopathology (fat deposition and apoptosis), (5) biochemical assays (reproductive hormones, oxidative stress markers, and inflammatory cytokines), and (6) molecular analyses (mRNA sequencing and qPCR validation of differentially expressed genes).Results: 4-HIL treatment improved metabolic parameters, including reduced weight gain, enhanced glucose tolerance, and optimized blood serum lipids, compared to HFD controls. Treated mice exhibited superior sperm quality with increased count and concentration, reduced histomorphological abnormalities in the testis, and attenuated oxidative stress and inflammation. Furthermore, the key spermatogenic gene expressions, including spem1 and spata24, were significantly optimized in the testes of mice treated with 4-HIL compared to those of untreated mice (HFD group).Conclusion: This study demonstrates that 4-HIL therapy ameliorates obesity-induced testicular dysfunction and improves fertility markers in mice. The beneficial effects of this compound on metabolic parameters, sperm quality, and spermatogenic gene expression suggest its potential as a therapeutic agent for obesity-related male infertility. Further research is warranted to elucidate the underlying mechanisms and assess the clinical translatability of these findings.
研究领域:
内分泌学
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生殖生物学
·
药理学
·
分子生物学
·
营养学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
REPRODUCTIVE BIOMEDICINE ONLINE
·
2020
·
IF 3.218
Xiaoyan Wan,Xiaomei He,Qian Liu,Peng Duan,Honggang Li
Research question Frequent and mild scrotal heat stress (fmSHS) often occurs in humans. The aim of this study was to determine the impact of fmSHS on natural fertility , the IVF–embryo transfer (IVF–ET) process and the offspring sex ratio. Design Male mice were randomly divided into four groups: no scrotal heat stress (SHS) (controls) and those subjected to SHS at 37°C, 39°C or 41°C for 30 min once a week for 5 consecutive weeks. The testis, epididymis and sperm quality were assessed to evaluate the effects of different degrees of SHS, to establish an fmSHS model. Then, natural fertility, IVF–embryo transfer (IVF–ET) results, embryo development, offspring sex ratio and the X/Y chromosome-bearing sperm ratio were examined. Results SHS at 39°C and 41°C caused mild impairment to spermatozoa , leading to a phenotype similar to oligoasthenozoospermia in humans. Given that most SHS conditions in humans are close to body temperature, SHS of 39°C was adopted to build the fmSHS model. fmSHS reduced the fertilization rate, impaired on-time development and reduced the implantation rate of the embryos in the IVF–ET process, but it did not affect the development or function of blastocysts . The fmSHS mice produced more Y chromosome-bearing spermatozoa and propagated more male offspring. Conclusions fmSHS not only reduced the fertilization ability of spermatozoa but also influenced their function beyond fertilization, in addition to changing the offspring sex ratio. These results may help to shed new light on the infertility treatment of males with scrotal heat risk and the health concerns of offspring propagated from these fathers.
研究领域:
生殖生物学
·
男科学
·
胚胎学
✓ 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）