亚慢性摄入环境相关浓度的砷会导致成年 Wistar 大鼠前列腺组织病变和氧化应激。

IF 3.3 4区 医学 Q2 REPRODUCTIVE BIOLOGY Reproductive toxicology Pub Date : 2024-06-22 DOI:10.1016/j.reprotox.2024.108647
John L.P. Coimbra , Gabriel Campolina-Silva , Daniel F. Lair , Luiz O. Guimarães-Ervilha , Ana C.F. Souza , Cleida A. Oliveira , Guilherme M.J. Costa , Mariana Machado-Neves
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引用次数: 0

摘要

前列腺是老年男性发生增生和癌症的主要部位之一。许多因素已被证实会破坏前列腺的平衡,包括暴露于环境污染物。砷是一种金属类化合物,普遍存在于土壤、空气和水中,人类会通过非自愿摄入受污染的饮用水和食物而中毒,并通过增加氧化应激反应而产生有害影响。本研究旨在探讨长期暴露于环境相关浓度的砷对成年 Wistar 大鼠前列腺生物学的影响。30 只 80 天大的雄性大鼠被分为三个实验组。对照组大鼠饮用过滤水,而砷组大鼠则每天摄入 1mgL-1 和 10mgL-1 亚砷酸钠形式的砷。砷溶液在饮用水中自由供应,持续八周。我们的研究结果表明,1 毫克/升-1 和 10 毫克/升-1 的砷可使前列腺发生良性和癌前组织病理学变化。摄入 1 毫克/升-1 的砷只会降低 SOD 活性,而 10 毫克/升-1 的砷则会降低前列腺组织中 SOD 和 CAT 的活性,最终导致产生大量 MDA。然而,这些剂量并不影响前列腺内 DHT 和雌二醇的水平。总之,通过饮用水接触环境相关浓度的砷会诱发成年大鼠前列腺组织学和氧化应激相关变化,从而加强砷接触与前列腺疾病之间的联系。
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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Subchronic intake of arsenic at environmentally relevant concentrations causes histological lesions and oxidative stress in the prostate of adult Wistar rats

The prostate gland is one of the main sites of hyperplasia and cancer in elderly men. Numerous factors have been demonstrated to disrupt prostate homeostasis, including exposure to environmental pollutants. Arsenic is a metalloid found ubiquitously in soil, air, and water, which favors human poisoning through the involuntary intake of contaminated drinking water and food and has harmful effects by increasing the oxidative stress response. This study aimed to investigate the effects of prolonged exposure to arsenic at environmentally relevant concentrations on the prostate biology of adult Wistar rats. Thirty 80-day-old male rats were divided into three experimental groups. Rats from the control group received filtered water, whereas animals from the arsenic groups ingested 1 mg L−1 and 10 mg L−1 of arsenic, in the form of sodium arsenite, daily. The arsenic solutions were provided ad libitum in the drinking water for eight weeks. Our results showed that 1 mg L−1 and 10 mg L−1 of arsenic made the prostate susceptible to evolving benign and premalignant histopathological changes. While the ingestion of 1 mg L−1 of arsenic reduced SOD activity only, 10 mg L−1 diminished SOD and CAT activity in the prostate tissue, culminating in high MDA production. These doses, however, did not affect the intraprostatic levels of DHT and estradiol. In conclusion, exposure to arsenic at environmentally relevant concentrations through drinking water induces histological and oxidative stress-related changes in the prostate of adult rats, strengthening the between arsenic exposure and prostate disorders.

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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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