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Published on: September 26, 2020
Thymoquinone and diallyl sulfide protect against fipronil-induced oxidative injury in rats
Mohamed M Abdel-Daim1, Hazem M Shaheen2, Abdelrahman Ibrahim Abushouk3
1Pharmacology Department, Faculty of Veterinary Medicine, Suez Canal University, Ismailia, 41522, Egypt. Abdeldaim.m@vet.suez.edu.eg.
Abstract:
Fipronil (FPN) is a phenylpyrazole insecticide, widely used for agricultural and veterinary activities. Early reports indicated that FIP organ toxicity is primarily mediated by the induction of oxidative stress. Both thymoquinone (TQ) and diallyl sulfide (DAS) are natural antioxidants with established health benefits. This study investigated the potential ameliorative effects of DAS and TQ against FPN-induced toxicity in rats. Thirty-two male Wistar rats (150-180 g) were randomized into four treatment groups, receiving (I) saline, (II) FPN (10 mg/kg bw), (III) FPN with DAS (200 mg/kg bw), and (IV) FPN with TQ (10 mg/kg bw). All treatments were administered once daily for 28 days. The results showed that compared to the control rats, FPN-treated rats had significantly increased (p < 0.05) serum levels of uric acid, urea, creatinine, cholesterol, aspartate transferase, alanine transferase, alkaline phosphatase, lactate dehydrogenase, and γ-glutamyl transferase. Moreover, FPN significantly reduced (p < 0.05) the serum levels of total proteins, albumin, and triglycerides. In addition, compared with the control group, FPN-treated rats had significantly elevated (p < 0.05) malondialdehyde and nitric oxide levels, as well as significantly reduced glutathione concentration and activities of glutathione peroxidase, superoxide dismutase, and catalase enzymes in the hepatic, renal, and brain tissues. Cotreatment with DAS or TQ significantly ameliorated (p < 0.05) the FPN-induced alterations in all the previously mentioned parameters with more frequent restoration of normal control ranges in the TQ group. In conclusion, both DAS and TQ alleviated the oxidative injury of FPN, probably by enhancing tissue antioxidant defenses.
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