Thymoquinone attenuates dimethoate induced hepatic and testicular genotoxicity in rats | ||||
| Kafrelsheikh Veterinary Medical Journal | ||||
| Article 6, Volume 18, Issue 2, October 2020, Page 25-32 PDF (684.44 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/kvmj.2020.40514.1010 | ||||
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| Authors | ||||
Fatma Zakzook  ; Hanaa Hegazy; Tarek Yosef; Ghada Gomaa
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| Department of Forensic Medicine, Faculty of Veterinary Medicine, Kafrelsheikh University | ||||
| Abstract | ||||
| Background: Dimethoate (DM) is an organophosphate insecticide widely used on crops in Egyptian fields. DM has many toxic impacts on non-target organisms especially mammals. Objective: This study aimed to evaluate therole of thymoquinone (TQ) against DM-induced hepatic and testicular subchronic genotoxicity. Methods: Forty- eight rats were randomly divided into 6 groups each of eight animals. Group 1 served as the normal control received distilled water; Group 2 was given DM; Group 3 received DM+TQ; Group 4 was treated by TQ; Group 5 was supplemented with DM+ olive oil (as a vehicle); and Group 6 was given olive oil. Oxidative/antioxidant status was assessed by quantification of malondialdehyde (MDA) levels and superoxide dismutase (SOD) and catalase (CAT) activities. Genotoxicity and apoptosis in the liver and testis were evaluated using the comet assay and immunohistochemical expression of caspase3 and Bax, respectively. Results: Significant DNA damage, marked histopathological changes in liver and testis, intense nuclear and cytoplasmic immune-expression of caspase 3 and Bax, significant decreases in catalase (CAT) and superoxide dismutase (SOD) activities and significant increase in malondialdehyde (MDA) levels were observed in DM-treated rats as compared to the control group. Concomitant treatment of TQ with DM drastically alleviated all the above-mentioned alterations. Conclusion: These findings suggest that TQ exhibits an outstanding ameliorative role against DM-induced hepatic and testicular genotoxicity in rats through the mitigation of oxidative stress and apoptosis. | ||||
| Keywords | ||||
| Apoptosis; Dimethoate; Genotoxicity; Oxidative stress; Thymoquinone | ||||
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