Mechanisms and rescue measures of female ovarian dysfunction induced by environmental endocrine chemicals: A review

IF 3.3 4区 医学 Q2 REPRODUCTIVE BIOLOGY
Jinglei Zhang , Nan Zhang , Qingyun Mai , Canquan Zhou
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Abstract

Environmental endocrine chemicals (EDCs) constitute a class of exogenous chemicals with the capacity to imitate or impede the processes of synthesis, secretion, transport, conjugation, reaction, and metabolism of natural hormones in living organisms. They elicit a broad spectrum of physiological effects, which may either mirror those of natural hormones or exhibit anti-natural characteristics. Prolonged exposure to EDCs has been demonstrated to exert significant effects on animal reproduction and development. It is noteworthy that the female reproductive system is more susceptible to the effects of EDCs than the male reproductive system. EDCs have the potential to cause significant damage to the structure and function of the female reproductive organs, and have been linked to an increased incidence of various tumors in the female reproductive system, including ovarian cancer. A growing body of evidence suggests that exposure to EDCs affects reproduction in five main ways: competitively binding to cell membrane-specific receptors, disruption of cellular signaling within germ cells, intracellular imbalance between reactive oxygen species and antioxidants, alteration of epigenetic modifications, and control of early apoptosis. Nevertheless, the same in vivo and in vitro studies have indicated that the reproductive toxicity produced by EDCs can also be attenuated in a multitude of ways, such as by antioxidants, hormones, and compensatory mechanisms of signal transduction. Through comprehensive analysis of epidemiological studies, laboratory experiments, and clinical observations, this review details the mechanisms of the effects of EDCs leading to ovarian dysfunction and proposes a series of strategies to prevent EDCs exposure.
环境内分泌化学物质诱发女性卵巢功能障碍的机制及抢救措施综述。
环境内分泌化学物质(Environmental endocrine chemicals, EDCs)是一类具有模仿或阻碍生物体内天然激素的合成、分泌、转运、结合、反应和代谢过程的外源性化学物质。它们引发了广泛的生理效应,这些效应可能反映了天然激素的作用,也可能表现出反自然的特征。长期暴露于EDCs已被证明对动物的繁殖和发育产生重大影响。值得注意的是,女性生殖系统比男性生殖系统更容易受到EDCs的影响。EDCs有可能对女性生殖器官的结构和功能造成重大损害,并与女性生殖系统中各种肿瘤(包括卵巢癌)的发病率增加有关。越来越多的证据表明,暴露于EDCs以五种主要方式影响生殖:与细胞膜特异性受体的竞争性结合,生殖细胞内细胞信号传导的破坏,细胞内活性氧和抗氧化剂之间的不平衡,表观遗传修饰的改变,以及早期凋亡的控制。然而,同样的体内和体外研究表明,EDCs产生的生殖毒性也可以通过多种方式减弱,例如抗氧化剂、激素和信号转导的补偿机制。本文通过流行病学研究、实验室实验和临床观察的综合分析,详细阐述了EDCs导致卵巢功能障碍的作用机制,并提出了一系列预防EDCs暴露的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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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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