膳食蛋白质缺乏加剧了全氟己烷磺酸(PFHxS)诱导的雌性大鼠生殖异常和代谢紊乱

IF 2.8 4区 医学 Q2 REPRODUCTIVE BIOLOGY
Suramya, Mehjbeen Javed, Anuradha Mangla, Suraj Kumar, Shaesta Shahid, Humaira Naaz Bhutto, Shahzad Ahmad, Basir Ahmad, Sheikh Raisuddin
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引用次数: 0

摘要

全氟己烷磺酸(PFHxS)是一种持久性环境污染物,与若干健康问题有关。人类主要通过摄入接触PFHxS。研究表明,缺乏必需营养素的饮食可能会对化学物质的毒性结果产生混淆效应。我们评估了PFHxS暴露对维持蛋白质缺乏饮食的动物生殖损伤的潜在影响。雌性Wistar大鼠(n = 6)分为对照组和治疗组(5 ppm和25 ppm PFHxS,蛋白质缺乏组,蛋白质缺乏+5 ppm PFHxS和蛋白质缺乏+25 ppm PFHxS)。PFHxS暴露于25 ppm和蛋白质缺乏+ 25 ppm的PFHxS分别显示55.56% %和78.77 %的紊乱,破坏了发情周期,增加了发情期的持续时间。有显著海拔(P & lt; 0.01)在LH / FSH比和减少睾酮(P & lt; 0.01),雌二醇(P & lt; 0.01)和孕酮(P & lt; 0.001)在蛋白质不足+ 25 ppm PFHxS组。蛋白缺乏+ 25 ppm PFHxS组脂质谱参数高阶增加。然而,高密度脂蛋白在这组降低。蛋白质缺乏+ 25 ppm PFHxS组动物也显示出高水平的氧化应激。组织病理学结果显示,蛋白缺乏+ 25 ppm PFHxS组卵巢出现囊性卵泡和卵膜细胞变性,子宫肌层和子宫内膜区域明显减少(P <; 0.01)。与单独的任何一个因素相比,蛋白质缺乏和PFHxS暴露的综合影响造成了更大的生殖毒性,这意味着营养不良人群的生殖功能更容易受到环境污染物的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dietary protein deficiency exacerbates perfluorohexane sulfonate (PFHxS)-induced reproductive abnormalities and metabolic disruptions in female rats
Perfluorohexane sulfonate (PFHxS) is a persistent environmental contaminant linked with several health implications. Humans are exposed to PFHxS mainly through ingestion. Studies have reported that a diet deficient in essential nutrients may have confounding effect on the toxicity outcome of chemicals. We evaluated the potential impact of PFHxS exposure on the reproductive damage in animals maintained on the diet deficient in protein. Female Wistar rats (n = 6) were divided as controls and treatment groups (5 ppm and 25 ppm PFHxS, protein deficient, protein deficient +5 ppm PFHxS and protein deficient +25 ppm PFHxS). PFHxS exposure disrupted the estrous cycle with an increased duration of the diestrus stage at 25 ppm and protein deficient + 25 ppm PFHxS showing 55.56 % and 78.77 % disorder, respectively. There was a significant elevation (P < 0.01) in LH/FSH ratio and reduction in testosterone (P < 0.01), estradiol (P < 0.01), and progesterone (P < 0.001) in protein deficient + 25 ppm PFHxS group. A high order of increase in lipid profile parameters was found in protein deficient + 25 ppm PFHxS group. However, high-density lipoprotein decreased in this group. Protein deficient + 25 ppm PFHxS group animals also revealed high level of oxidative stress. Histopathological findings revealed the presence of cystic follicles and theca cell degeneration in ovaries in the protein deficient + 25 ppm PFHxS group with a significant decrease (P < 0.01) in the myometrium and endometrial area of uterus. The combined effect of protein deficiency and PFHxS exposure caused a greater reprotoxicity compared to either factor alone implying an increased vulnerability of reproductive function in malnourished populations to environmental contaminants.
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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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