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  • Environmental Toxicology 2016

    Rights statement: This is the peer reviewed version of the following article: Duan, P., Hu, C., Butler, H. J., Quan, C., Chen, W., Huang, W., Tang, S., Zhou, W., Yuan, M., Shi, Y., Martin, F. L. and Yang, K. (2017), 4-Nonylphenol induces disruption of spermatogenesis associated with oxidative stress-related apoptosis by targeting p53-Bcl-2/Bax-Fas/FasL signaling. Environ. Toxicol., 32: 739–753. doi:10.1002/tox.22274 which has been published in final form at http://onlinelibrary.wiley.com/doi/10.1002/tox.22274/abstract This article may be used for non-commercial purposes in accordance With Wiley Terms and Conditions for self-archiving.

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4-Nonylphenol induces disruption of spermatogenesis associated with oxidative stress-related apoptosis by targeting p53-Bcl-2/Bax-Fas/FasL signaling

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4-Nonylphenol induces disruption of spermatogenesis associated with oxidative stress-related apoptosis by targeting p53-Bcl-2/Bax-Fas/FasL signaling. / Duan, Peng; Hu, Chunhui; Butler, Holly; Quan, Chao; Chen, Wei; Huang, Wenting ; Tang, Sha; Zhou, Wei; Yuan, Meng; Shi, Yuqin; Martin, Francis Luke; Yang, Kedi.

In: Environmental Toxicology, Vol. 32, No. 3, 03.2017, p. 739-753.

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Duan, Peng ; Hu, Chunhui ; Butler, Holly ; Quan, Chao ; Chen, Wei ; Huang, Wenting ; Tang, Sha ; Zhou, Wei ; Yuan, Meng ; Shi, Yuqin ; Martin, Francis Luke ; Yang, Kedi. / 4-Nonylphenol induces disruption of spermatogenesis associated with oxidative stress-related apoptosis by targeting p53-Bcl-2/Bax-Fas/FasL signaling. In: Environmental Toxicology. 2017 ; Vol. 32, No. 3. pp. 739-753.

Bibtex

@article{9605fcf9742c4556bba2cc391e5c527e,
title = "4-Nonylphenol induces disruption of spermatogenesis associated with oxidative stress-related apoptosis by targeting p53-Bcl-2/Bax-Fas/FasL signaling",
abstract = "4-Nonylphenol (NP) is a ubiquitous environmental chemical with estrogenic activity. Our aim was to test the hypothesis that pubertal exposure to NP leads to testicular dysfunction. Herein, 24 7-week-old rats were randomly divided into four groups and treated with NP (0, 25, 50, or 100 mg/kg body weight every 2 days for 20 consecutive days) by intraperitoneal injection. Compared to untreated controls, the parameters of sperm activation rate, curvilinear velocity, average path velocity, and swimming velocity were significantly lower at doses of 100 mg/kg, while sperm morphological abnormalities were higher, indicating functional disruption and reduced fertilization potential. High exposure to NP (100 mg/kg) resulted in disordered arrangement of spermatoblasts and reduction of spermatocytes in seminiferous tubules, while tissues exhibited a marked decline in testicular fructose content and serum FSH, LH, and testosterone levels. Oxidative stress was induced by NP (50 or 100 mg/kg) as evidenced by elevated MDA, decreased SOD and GSH-Px, and inhibited antioxidant gene expression (CAT, GPx, SOD1, and CYP1B1). In addition, NP treatment decreased proportions of Ki-67-positive cells and increased apoptosis in a dose-dependent manner. Rats treated with 100 mg/kg NP exhibited significantly increased mRNA expression of caspase-1, -2, -9, and -11, decreased caspase-8 and PCNA1 mRNA expression, downregulation of Bcl-2/Bax ratios and upregulation of Fas, FasL, and p53 at the protein and mRNA levels. Taken together, NP-induced apoptosis, hormonal deficiencies, and depletion of fructose potentially impairs spermatogenesis and sperm function. p53-independent Fas/FasL-Bax/Bcl-2 pathways may be involved in NP-induced oxidative stress-related apoptosis. ",
keywords = "apoptosis, endocrine disruptor, 4-nonylphenol, oxidative stress, spermatogenesis, testicular dysfunction",
author = "Peng Duan and Chunhui Hu and Holly Butler and Chao Quan and Wei Chen and Wenting Huang and Sha Tang and Wei Zhou and Meng Yuan and Yuqin Shi and Martin, {Francis Luke} and Kedi Yang",
note = "This is the peer reviewed version of the following article: Duan, P., Hu, C., Butler, H. J., Quan, C., Chen, W., Huang, W., Tang, S., Zhou, W., Yuan, M., Shi, Y., Martin, F. L. and Yang, K. (2017), 4-Nonylphenol induces disruption of spermatogenesis associated with oxidative stress-related apoptosis by targeting p53-Bcl-2/Bax-Fas/FasL signaling. Environ. Toxicol., 32: 739–753. doi:10.1002/tox.22274 which has been published in final form at http://onlinelibrary.wiley.com/doi/10.1002/tox.22274/abstract This article may be used for non-commercial purposes in accordance With Wiley Terms and Conditions for self-archiving.",
year = "2017",
month = mar,
doi = "10.1002/tox.22274",
language = "English",
volume = "32",
pages = "739--753",
journal = "Environmental Toxicology",
issn = "1520-4081",
publisher = "John Wiley and Sons Inc.",
number = "3",

}

RIS

TY - JOUR

T1 - 4-Nonylphenol induces disruption of spermatogenesis associated with oxidative stress-related apoptosis by targeting p53-Bcl-2/Bax-Fas/FasL signaling

AU - Duan, Peng

AU - Hu, Chunhui

AU - Butler, Holly

AU - Quan, Chao

AU - Chen, Wei

AU - Huang, Wenting

AU - Tang, Sha

AU - Zhou, Wei

AU - Yuan, Meng

AU - Shi, Yuqin

AU - Martin, Francis Luke

AU - Yang, Kedi

N1 - This is the peer reviewed version of the following article: Duan, P., Hu, C., Butler, H. J., Quan, C., Chen, W., Huang, W., Tang, S., Zhou, W., Yuan, M., Shi, Y., Martin, F. L. and Yang, K. (2017), 4-Nonylphenol induces disruption of spermatogenesis associated with oxidative stress-related apoptosis by targeting p53-Bcl-2/Bax-Fas/FasL signaling. Environ. Toxicol., 32: 739–753. doi:10.1002/tox.22274 which has been published in final form at http://onlinelibrary.wiley.com/doi/10.1002/tox.22274/abstract This article may be used for non-commercial purposes in accordance With Wiley Terms and Conditions for self-archiving.

PY - 2017/3

Y1 - 2017/3

N2 - 4-Nonylphenol (NP) is a ubiquitous environmental chemical with estrogenic activity. Our aim was to test the hypothesis that pubertal exposure to NP leads to testicular dysfunction. Herein, 24 7-week-old rats were randomly divided into four groups and treated with NP (0, 25, 50, or 100 mg/kg body weight every 2 days for 20 consecutive days) by intraperitoneal injection. Compared to untreated controls, the parameters of sperm activation rate, curvilinear velocity, average path velocity, and swimming velocity were significantly lower at doses of 100 mg/kg, while sperm morphological abnormalities were higher, indicating functional disruption and reduced fertilization potential. High exposure to NP (100 mg/kg) resulted in disordered arrangement of spermatoblasts and reduction of spermatocytes in seminiferous tubules, while tissues exhibited a marked decline in testicular fructose content and serum FSH, LH, and testosterone levels. Oxidative stress was induced by NP (50 or 100 mg/kg) as evidenced by elevated MDA, decreased SOD and GSH-Px, and inhibited antioxidant gene expression (CAT, GPx, SOD1, and CYP1B1). In addition, NP treatment decreased proportions of Ki-67-positive cells and increased apoptosis in a dose-dependent manner. Rats treated with 100 mg/kg NP exhibited significantly increased mRNA expression of caspase-1, -2, -9, and -11, decreased caspase-8 and PCNA1 mRNA expression, downregulation of Bcl-2/Bax ratios and upregulation of Fas, FasL, and p53 at the protein and mRNA levels. Taken together, NP-induced apoptosis, hormonal deficiencies, and depletion of fructose potentially impairs spermatogenesis and sperm function. p53-independent Fas/FasL-Bax/Bcl-2 pathways may be involved in NP-induced oxidative stress-related apoptosis.

AB - 4-Nonylphenol (NP) is a ubiquitous environmental chemical with estrogenic activity. Our aim was to test the hypothesis that pubertal exposure to NP leads to testicular dysfunction. Herein, 24 7-week-old rats were randomly divided into four groups and treated with NP (0, 25, 50, or 100 mg/kg body weight every 2 days for 20 consecutive days) by intraperitoneal injection. Compared to untreated controls, the parameters of sperm activation rate, curvilinear velocity, average path velocity, and swimming velocity were significantly lower at doses of 100 mg/kg, while sperm morphological abnormalities were higher, indicating functional disruption and reduced fertilization potential. High exposure to NP (100 mg/kg) resulted in disordered arrangement of spermatoblasts and reduction of spermatocytes in seminiferous tubules, while tissues exhibited a marked decline in testicular fructose content and serum FSH, LH, and testosterone levels. Oxidative stress was induced by NP (50 or 100 mg/kg) as evidenced by elevated MDA, decreased SOD and GSH-Px, and inhibited antioxidant gene expression (CAT, GPx, SOD1, and CYP1B1). In addition, NP treatment decreased proportions of Ki-67-positive cells and increased apoptosis in a dose-dependent manner. Rats treated with 100 mg/kg NP exhibited significantly increased mRNA expression of caspase-1, -2, -9, and -11, decreased caspase-8 and PCNA1 mRNA expression, downregulation of Bcl-2/Bax ratios and upregulation of Fas, FasL, and p53 at the protein and mRNA levels. Taken together, NP-induced apoptosis, hormonal deficiencies, and depletion of fructose potentially impairs spermatogenesis and sperm function. p53-independent Fas/FasL-Bax/Bcl-2 pathways may be involved in NP-induced oxidative stress-related apoptosis.

KW - apoptosis

KW - endocrine disruptor

KW - 4-nonylphenol

KW - oxidative stress

KW - spermatogenesis

KW - testicular dysfunction

U2 - 10.1002/tox.22274

DO - 10.1002/tox.22274

M3 - Journal article

VL - 32

SP - 739

EP - 753

JO - Environmental Toxicology

JF - Environmental Toxicology

SN - 1520-4081

IS - 3

ER -