Kaur Simranjeet, Singla Neha, Dhawan D K
a Department of Biophysics , Panjab University , Chandigarh , India.
Drug Chem Toxicol. 2019 Mar;42(2):220-230. doi: 10.1080/01480545.2019.1569022. Epub 2019 Feb 12.
Chlorpyrifos (CPF) has been considered as one of the most potent organophosphates and is linked to several neurological disorders. On the other hand, Quercetin is a vital plant flavanoid and has been reported to regulate a number of physiological processes in the central nervous system. The present study was conducted to investigate the protective potential of quercetin during chlorpyrifos induced neurotoxicity. Female Wistar rats weighing 150-200 g were divided into four different groups viz: Normal control, CPF treated (13.5 mg/kg.b.wt. every alternate day), Quercetin treated (50 mg/kg.b.wt./day) and combined CPF and quercetin-treated. All the treatments were carried out for a total duration of eight weeks. Chlorpyrifos treatment showed significant alterations in the cognitive behavior and motor activities of rats, which were appreciably improved upon simultaneous supplementation with quercetin. Further, CPF treatment caused a significant inhibition in the enzyme activities of acetylcholinesterase and choline acetyltransferase, but caused an increase in the levels of acetylcholine in the brain. Further, chlorpyrifos exposure significantly elevated the levels of lipid peroxidation and protein carbonyl contents as well as the activities of catalase, superoxide dismutase, which were interestingly found to be decreased following co-treatment with quercetin. In contrast, CPF treatment decreased the activities of glutathione reductase, transferase, as well as levels of reduced and total glutathione in both the cerebrum and cerebellum but co-administration of quercetin, increased these levels. Chlorpyrifos treatment altered the neuro-histoarchitecture, which showed improvement upon quercetin supplementation. Hence, this study suggests that quercetin can be used as a prophylactic intervention to prevent CPF induced neurotoxicity.
毒死蜱(CPF)被认为是最具毒性的有机磷酸酯之一,与多种神经疾病有关。另一方面,槲皮素是一种重要的植物类黄酮,据报道可调节中枢神经系统中的许多生理过程。本研究旨在探讨槲皮素在毒死蜱诱导的神经毒性中的保护潜力。将体重150 - 200克的雌性Wistar大鼠分为四组:正常对照组、毒死蜱处理组(每隔一天13.5毫克/千克体重)、槲皮素处理组(50毫克/千克体重/天)以及毒死蜱和槲皮素联合处理组。所有处理共持续八周。毒死蜱处理使大鼠的认知行为和运动活动出现显著改变,同时补充槲皮素后这些改变得到明显改善。此外,毒死蜱处理导致乙酰胆碱酯酶和胆碱乙酰转移酶的酶活性显著抑制,但使脑中乙酰胆碱水平升高。此外,毒死蜱暴露显著提高了脂质过氧化水平和蛋白质羰基含量以及过氧化氢酶、超氧化物歧化酶的活性,有趣的是,与槲皮素联合处理后这些指标有所下降。相反,毒死蜱处理降低了大脑和小脑中谷胱甘肽还原酶、转移酶的活性以及还原型和总谷胱甘肽水平,但槲皮素联合给药后这些水平升高。毒死蜱处理改变了神经组织架构,补充槲皮素后有所改善。因此,本研究表明槲皮素可作为一种预防性干预措施来预防毒死蜱诱导的神经毒性。