Department of Zoology, Faculty of Science, Cairo University, Cairo, Egypt.
Sci Rep. 2020 Nov 11;10(1):19544. doi: 10.1038/s41598-020-76638-6.
Insecticides and other agrochemicals have become indispensable components of the agricultural system to ensure a notable increase in crop yield and food production. As a natural consequence, chemical residues result in significantly increased contamination of both terrestrial and aquatic ecosystems. The present study evaluated the teratogenic, genotoxic, and oxidative stress effects of residual-level lufenuron exposure on pregnant rats during the organogenesis gestational period of both mother and fetus. The tested dams were divided into three groups; control (untreated), low-dose group (orally administered with 0.4 mg/kg lufenuron) and high-dose group (orally administered with 0.8 mg/kg lufenuron). The dams of the two treatment groups showed teratogenic abnormalities represented by the asymmetrical distribution of fetuses in both uterine horns, accompanied by observed resorption sites and intensive bleeding in the uterine horns, whereas their fetuses suffered from growth retardation, morphologic malformations, and skeletal deformations. Histologic examination of the liver and kidney tissues obtained from mothers and fetuses after lufenuron exposure revealed multiple histopathologic changes. DNA fragmentation and cell cycle perturbation were also detected in the liver cells of lufenuron-treated pregnant dams and their fetuses through comet assay and flow cytometry, respectively. Moreover, lufenuron-induced oxidative stress in the liver of mothers and fetuses was confirmed by the increased malondialdehyde levels and decreased levels of enzymatic antioxidants (glutathione peroxidase and superoxide dismutase). Taken together, it can be concluded that lufenuron has a great potential in exerting teratogenic, genotoxic, and oxidative stresses on pregnant rats and their fetuses upon chronic exposure to residual levels during the organogenesis gestational period. The obtained results in the present study imply that women and their fetuses may have the same risk.
杀虫剂和其他农用化学品已成为农业系统中不可或缺的组成部分,以确保显著提高作物产量和粮食生产。作为一个自然的结果,化学残留导致陆地和水生生态系统的污染显著增加。本研究评估了残留水平的 lufenuron 暴露对怀孕大鼠在母体和胎儿器官发生期间的致畸、遗传毒性和氧化应激影响。测试的孕鼠分为三组:对照组(未处理)、低剂量组(口服给予 0.4mg/kg lufenuron)和高剂量组(口服给予 0.8mg/kg lufenuron)。两个治疗组的孕鼠表现出致畸异常,表现为胎儿在两个子宫角中的不对称分布,伴有观察到的吸收部位和子宫角内的密集出血,而其胎儿则表现出生长迟缓、形态畸形和骨骼畸形。对暴露于 lufenuron 后的母亲和胎儿的肝脏和肾脏组织进行组织学检查,发现了多种组织病理学变化。通过彗星试验和流式细胞术分别检测到 lufenuron 处理的孕鼠及其胎儿的肝细胞中的 DNA 片段化和细胞周期扰动。此外,通过丙二醛水平的升高和酶抗氧化剂(谷胱甘肽过氧化物酶和超氧化物歧化酶)水平的降低,证实了 lufenuron 在母亲和胎儿肝脏中诱导的氧化应激。综上所述,可以得出结论,lufenuron 在慢性暴露于残留水平期间在器官发生期间对怀孕大鼠及其胎儿具有很大的致畸、遗传毒性和氧化应激潜力。本研究中的结果表明,妇女及其胎儿可能面临相同的风险。