4.7 Article

Effect of atrazine on testicular toxicity involves accommodative disorder of xenobiotic metabolizing enzymes system and testosterone synthesis in European quail (Coturnix coturnix)

Journal

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 268, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2023.115716

Keywords

Atrazine; European quail; Endocrine disruptor; Cytochrome P450 enzyme; Reproductive toxicity

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The wide use of atrazine has raised concerns about its negative impact on reproduction. This study examined the reproductive toxicity and metabolic disorders caused by atrazine exposure in European quail. The results showed that high doses of atrazine significantly decreased testicular coefficient and acted as a potent CYP disruptor. Additionally, atrazine disrupted hormone balance by affecting the expression of hormones in the gonad axis.
Due to the wide use of atrazine (ATR), the concern has increased regarding the negative impact of ATR on reproduction. Nevertheless, the reproductive effects caused by different exposure concentrations and the severity of toxic damage are poorly understood. In organisms, ATR is metabolized and degraded through phase II enzyme systems, and changes in cytochrome P450 (CYP) enzymes may have a regulatory role in the harm of ATR. However, less information is available on the induction of CYPs by ATR in avian organisms, and even less on its effects on the testis. Birds are exposed to ATR mainly through food residues and contaminated water, the purpose of this study was to examine reproductive toxicity by different exposure concentrations and elaborate metabolic disorders caused by ATR in European quail (Coturnix coturnix). In this study, the quail were given ATR at 50 mg/ kg, 250 mg/kg and 500 mg/kg by oral gavage for 45 days, and the testicular weight coefficients, histopathology and ultrastructure of testes, primary biochemical functions, sex steroid hormones, critical protein levels in the testosterone synthesis pathway, the expression of genes involved CYPs, gonad axis and nuclear receptors expression were investigated. Altogether, testicular coefficient decreased significantly in the high-dose group (1.22%) compared with the control group (3.03%) after 45 days of ATR exposure, and ATR is a potent CYP disruptor that acts through the NXRs and steroid receptor subfamily (APND, CAR, ERND and ER alpha) without a dose-dependent manner. Notably, ATR interfered with the homeostasis of hormones by triggering the expression of hormones on the gonad axis (LH and E2). These results suggest that exposure to ATR can cause testicular toxicity involving accommodative disorder of phase II enzyme and testosterone synthesis in European quail.

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