Suppressive effects of long-term exposure to P-nitrophenol on gonadal development, hormonal profile with disruption of tissue integrity, and activation of caspase-3 in male Japanese quail (Coturnix japonica).

Eman Ahmed,Mostafa Fayez,Kentaro Nagaoka,Haney Samir,Mohamed M Abdel-Daim,Gen Watanabe

doi:10.1007/s11356-015-4245-9

Abstract

P-Nitrophenol (PNP) is considered to be one of nitrophenol derivatives of diesel exhaust particles. PNP is a major metabolite of some organophosphorus compounds. PNP is a persistent organic pollutant as well as one of endocrine-disrupting compounds. Consequently, bioaccumulation of PNP potentiates toxicity. The objectives of the current study were to assess in vivo adverse effects of long-term low doses of PNP exposure on reproductive system during development stage. Twnety-eight-day-old male Japanese quails were orally administered different doses of PNP (0, 0.01, 0.1, 1 mg/kg body weight) daily for 2.5 months. Testicular histopathology, hormones, caspase-3 (CASP3), and claudin-1 (CLDN1) tight junction protein, as well as plasma hormones were analyzed. The results revealed that long-term PNP exposure caused testicular histopathological changes such as vacuolation of spermatogenic cell and spermatocyte with significant testicular and cloacal gland atrophy. PNP activated CASP3 enzyme that is an apoptosis-related cysteine peptidase. Besides, it disrupted the expression of CLDN1. Furthermore, a substantial decrease in plasma concentrations of luteinizing hormone (LH) and testosterone was observed after 2 and 2.5 months in the PNP-treated groups. Meanwhile, the pituitary LH did not significantly change. Site of action of PNP may be peripheral on testicular development and/or centrally on the hypothalamic–pituitary–gonadal axis through reduction of pulsatile secretion of gonadotrophin-releasing hormone. Consequently, it may reduce the sensitivity of the anterior pituitary gland to secrete LH. In conclusion, PNP induced profound endocrine disruption in the form of hormonal imbalance, induction of CASP3, and disruption of CLDN1 expression in the testis. Hence, it may hinder the reproductive processes.

Highlights

There is an increase in public and scientific communities’ attention concerning the effects of endocrine-disrupting chemicals on the reproductive and the endocrine systems
The expression of CLDN1, tight junctions (TJs) proteins were disturbed in the PNP-treated groups contrary to the control birds
As far as the researchers are aware, this is the first study aimed to measure the effect of long-term low doses of PNP administration on hormonal balance, caspase-3 (CASP3), and claudin-1 (CLDN1) expressions

Summary

Introduction

There is an increase in public and scientific communities’ attention concerning the effects of endocrine-disrupting chemicals on the reproductive and the endocrine systems. It is well known that the decline in human, livestock, and wildlife endocrine health is mainly caused by environmental pollution (Stone 1994). Many environmental chemicals have been experimentally demonstrated that they adversely affect the endocrine processes (Zhang et al 2013), known as Environ Sci Pollut Res (2015) 22:10930–10942 endocrine disruptors. Diesel exhaust particles (DEPs) have an environmental and occupational health concern (Taneda et al 2004). DEPs have become one of the main factors incriminated in various hazardous health problems for instance, reproductive dysfunction (Taneda et al 2004), lung cancer (Ichinose et al 1997), and bronchial asthma-like disease (Sagai et al 1993)

Objectives

Results

Conclusion