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  • RepTox2016

    Rights statement: This is the author’s version of a work that was accepted for publication in Reproductive Toxicology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Reproductive Toxicology, 62 2016 DOI: 10.1016/j.reprotox.2016.04.016

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Effects of 4-Nonylphenol on spermatogenesis and induction of testicular apoptosis through oxidative stress-related pathways

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<mark>Journal publication date</mark>1/07/2016
<mark>Journal</mark>Reproductive Toxicology
Volume62
Number of pages12
Pages (from-to)27-38
Publication statusPublished
Early online date22/04/16
Original languageEnglish

Abstract

This study tested the hypothesis that prepubertal exposure to 4-Nonylphenol (NP) affects reproductive function in male rats. Twenty-four rats at five-weeks-old were randomly divided into four groups and treated with NP at varying concentrations (0, 5, 20, and 60 mg/kg/2d) for thirty days by intra-peritoneal injection. 60 mg/kg NP induced spermatogenic degeneration and pronounced deficits in epididymal sperm count, motility and function, whereas potentially stimulatory effects were observed at 5 NP mg/kg. Moreover, 60 mg/kg NP resulted in a significant reduction in fructose, FSH and LH; induced apoptosis related to oxidative stress; inhibited mRNA and protein levels of Bcl-2 and PCNA; as well as the additional up-regulation of p53, Bax, Apaf-1, cytochrome c, cleaved-caspase-3, Fas and FasL expression. Our data suggest potentially hormetic effects of NP on spermatogenic function. High-dose NP impairs testicular development and function by reducing cell proliferation and inducing apoptosis involving oxidative stress-related p53-Bcl-2/Bax and −Fas/FasL pathways.

Bibliographic note

This is the author’s version of a work that was accepted for publication in Reproductive Toxicology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Reproductive Toxicology, 62 2016 DOI: 10.1016/j.reprotox.2016.04.016