Whole-body exposure to filtered fraction of diesel exhaust induced localized testicular damage through attenuated functional response of glutathione-s-transferase in adult male Wistar rats

IF 3.3 4区 医学 Q2 REPRODUCTIVE BIOLOGY Reproductive toxicology Pub Date : 2024-08-06 DOI:10.1016/j.reprotox.2024.108682
Swarnabha Sarkar , Aditya Dontham , Ravindran Revand , Abhishek Kandpal , Debabrata Dasgupta , Bahni Ray , Mayank Kumar , Asmita Patil
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Abstract

The possible vulnerability of the male reproductive system to environmental pollutants such as air pollution necessitates a thorough investigation of the underlying mechanisms involved in the dysregulation of male reproductive function. The present study was designed to investigate the influence of the filtered fraction of diesel exhaust (predominantly comprising gases) on male reproductive function in Wistar rat model. Adult male rats were randomly assigned into three groups (n=8/group): Control (unexposed) group (CG-A), the Clean air group in WBE chamber (CAG-A), and Filtered diesel exhaust group in WBE chamber (FDG-A). The exposure protocol for CAG-A and FDG-A was 6 h/day x 5d/week x 6 weeks,evaluation of sperm parameters, testicular histopathology, quantification of hormones (testosterone, LH, FSH, 17β-Estradiol, and prolactin), and GST levels were performed. Results showed that WBE to FDE leads to a significant decline in sperm concentration (p=0.008, CG-A vs FDG-A; p=0.014, CAG-A vs FDG-A), motility (p=0.008, CG-A vs FDG-A; p=0.029, CAG-A vs FDG-A), serum testosterone (p=0.024, CG-A vs FDG-A; p=0.007, CAG-A vs FDG-A), testicular testosterone (p=0.008, CG-A vs FDG-A; p=0.028, CAG-A vs FDG-A), 17β-Estradiol (p=0.007, CG-A vs FDG-A), and GST levels (p=0.0002, CG-A vs FDG-A; p=0.0019, CAG-A vs FDG-A). These findings demonstrate the disruption of testosterone-estradiol balance in the intratesticular milieu without significant alterations in other principal pituitary hormones in adult rats exposed to FDE. The predominant presence of gaseous components in FDE can cause testicular damage due to oxidative imbalance. This underscores the causality of FDE exposure and impaired male reproductive outcomes.

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成年雄性 Wistar 大鼠全身暴露于柴油废气的过滤馏分后,谷胱甘肽-S-转移酶的功能反应减弱,从而诱发局部睾丸损伤。
由于雄性生殖系统可能易受空气污染等环境污染物的影响,因此有必要深入研究导致雄性生殖功能失调的内在机制。本研究旨在调查柴油废气过滤部分(主要包括气体)对 Wistar 大鼠雄性生殖功能的影响。将成年雄性大鼠随机分为三组(n=8/组):对照(未暴露)组(CG-A)、WBE 室中的清洁空气组(CAG-A)和 WBE 室中的过滤柴油废气组(FDG-A)。CAG-A 和 FDG-A 的暴露方案为 6 小时/天 x 5 天/周 x 6 周,并对精子参数、睾丸组织病理学、激素(睾酮、LH、FSH、17β-雌二醇和催乳素)定量以及 GST 水平进行了评估。结果显示,WBE 对 FDE 会导致精子浓度(P=0.008,CG-A vs FDG-A;P=0.014,CAG-A vs FDG-A)、活力(P=0.008,CG-A vs FDG-A;P=0.029,CAG-A vs FDG-A)、血清睾酮(P=0.024,CG-A vs FDG-A;p=0.007,CAG-A vs FDG-A)、睾丸睾酮(p=0.008,CG-A vs FDG-A;p=0.028,CAG-A vs FDG-A)、17β-雌二醇(p=0.007,CG-A vs FDG-A)和 GST 水平(p=0.0002,CG-A vs FDG-A;p=0.0019,CAG-A vs FDG-A)。这些研究结果表明,暴露于溴化二苯醚的成年大鼠睾丸内环境中的睾酮-雌二醇平衡被打破,但其他主要垂体激素没有发生显著变化。在溴化二苯醚中主要存在的气体成分会因氧化失衡而导致睾丸损伤。这强调了接触溴化二苯醚与男性生殖功能受损之间的因果关系。
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来源期刊
Reproductive toxicology
Reproductive toxicology 生物-毒理学
CiteScore
6.50
自引率
3.00%
发文量
131
审稿时长
45 days
期刊介绍: Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine. All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.
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