Abstract
Objectives: The present study aimed to investigate the antioxidant activity of cerium oxide nanoparticles (CeNPs) against paraquat (PQ)-induced liver injury in rats. Methods: Thirty-two male rats were divided into four 8-member groups and treated intraperitoneally with PQ and/or CeNPs for 14 days. Group 1 received PQ (5 mg/kg/d), group 2 received CeNPs (15, 30, and 60 mg/kg/d), group 3 received a combination of PQ (5 mg/kg/d) and CeNPs (15, 30, and 60 mg/kg/d), and group 4 (control group) received saline solution. Serum samples along with liver tissue samples were collected from all the rats. Oxidative stress (OS) biomarkers including total antioxidant capacity, lipid peroxidation, total thiol groups, DNA damage, and nitric oxide levels were determined. Histological samples were also analyzed using hematoxylin and eosin staining slides. Results: Levels of oxidative stress and hepatic tissue damage were significantly higher in the PQ group compared to the control group. CeNPs at a dose of 15 mg/kg showed the antioxidant activity and compromised the PQ-induced damage. Conclusion: In the scenario tested in this study, CeNPs could reduce the levels of OS, as well as hepatic damage induced by PQ.
Highlights
Paraquat (PQ) (N, N′-dimethyl-4,4′-bipyridinium dichloride) is regarded as one of the most broadly-used herbicides worldwide
Total Antioxidant Capacity A statistically significant reduction was noted in total antioxidant capacity (TAC) for PQ group in comparison with the control group
Compared to the PQ group, a significant elevation in TAC was observed in the group receiving cerium oxide nanoparticles (CeNPs) (15, 30, and 60 mg/kg)
Summary
Paraquat (PQ) (N, N′-dimethyl-4,4′-bipyridinium dichloride) is regarded as one of the most broadly-used herbicides worldwide. PQ triggers harmful chemical reactions in various organs including lungs, liver, and kidneys [2,3]. Multiple-organ failures, mainly that of lungs [4,5], kidneys [6,7], and liver [8,9] are indicators of serious PQ poisoning. By interfering in the intracellular electron transfer systems of plants, PQ inhibits the reduction of NADP to NADPH through photosynthesis, thereby exerting the herbicidal activity [11]. This activity results in the formation of reactive oxygen species (ROS) such as superoxide anion, singlet oxygen, and hydroxyl and peroxyl radicals [12]. The high death rate following PQ poisoning has been ascribed to the absence of an antidote or operative treatment to ameliorate the harmful effects of this herbicide
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