Prenatal exposure to ethion caused maternal and foetal toxicity in rats

IF 3.3 4区 医学 Q2 REPRODUCTIVE BIOLOGY
Elizabeth Glanet Durom , V.A. Aneesha , Nerella Venkata Pavan Kumar , Ajmi Bin Azeez , M. Karikalan , Madhu C. Lingaraju , Subhashree Parida , Avinash G. Telang , Thakur Uttam Singh
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Abstract

Ethion is a class II moderately toxic organothiophosphate pesticide. The main objective of this study was to evaluate the maternal and foetal toxicity of ethion in rats. Pregnant rats were divided into 5 groups. Group I served as control. Group II, III, IV, and V were orally administered with 0.86, 1.71, 3.43, and 6.9 mg/kg of ethion respectively, from gestational day (GD) 6–19. Dams were sacrificed on GD 20. Maternal toxicity was assessed by body weight gain, foetal resorptions, oxidative stress, liver and kidney function tests, and histopathology. Foetal toxicity was assessed by physical status, gross, teratological and histopathological examination. Ethion caused dose-dependent reduction in maternal body weight gain, increased resorptions, and reduced gravid uterine weights. Elevated MDA levels and altered levels of GSH, SOD and catalase were recorded in pregnant dam serum and tissues. SGOT, SGPT, total bilirubin, urea, uric acid, and creatinine were elevated in ethion groups indicating liver and kidney toxicity. Histology of uterus revealed myometrial degeneration and mucosal gland atrophy in uterus of pregnant dams and degenerative changes in placenta. It showed histological alterations in liver, kidney, and lungs. There was reduction in the foetal body weights and placental weights, and degenerative changes in the foetal liver and kidney. Gross evaluation of foetuses showed subcutaneous hematoma. Skeletal evaluation showed partial ossification of skull bones, costal separation, and agenesis of tail vertebrae, sternebrae, metacarpals and metatarsals. The findings reveal that prenatal exposure to ethion caused maternal and foetal toxicity in rats.

大鼠产前接触乙硫磷会导致母体和胎儿中毒。
乙硫磷是一种第二类中毒性有机硫代磷酸农药。本研究的主要目的是评估乙硫磷对大鼠母体和胎儿的毒性。怀孕大鼠被分为 5 组。I 组为对照组。II、III、IV 和 V 组在妊娠期第 6 至 19 天分别口服 0.86、1.71、3.43 和 6.9 毫克/千克的乙硫磷。母鼠在妊娠期第 20 天被处死。母体毒性通过体重增加、胎儿畸形、氧化应激、肝肾功能测试和组织病理学进行评估。胎儿毒性通过身体状况、大体、畸形和组织病理学检查进行评估。乙硫磷会导致母体体重增加呈剂量依赖性减少、胎儿再发育增加和妊娠子宫重量减少。妊娠母体血清和组织中的 MDA 水平升高,GSH、SOD 和过氧化氢酶水平发生变化。乙硫磷组的 SGOT、SGPT、总胆红素、尿素、尿酸和肌酐升高,表明肝脏和肾脏中毒。子宫组织学检查显示,妊娠母体的子宫肌层退化,粘膜腺体萎缩,胎盘也发生了退行性变化。肝脏、肾脏和肺部也出现了组织学变化。胎儿体重和胎盘重量减少,胎儿肝脏和肾脏发生退行性变化。胎儿的大体评估显示有皮下血肿。骨骼评估显示颅骨部分骨化,肋骨分离,尾椎、胸骨、掌骨和跖骨发育不良。研究结果表明,妊娠期接触乙硫磷会导致大鼠母体和胎儿中毒。
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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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