Protective effects of thymoquinone against acrylamide-induced liver, kidney and brain oxidative damage in rats
Résumé
Acrylamide (AA), an industrial monomer, may cause multi-organ toxicity through induction of oxidative stress and inflammation. The antioxidant properties of thymoquinone (TQ), an active constituent of Nigella sativa, have been established before. The
aim of the current study was to assess the protective effects of TQ against AA-induced toxicity in rats. Forty-eight male Wistar
rats were divided into six groups each of eight rats. The first group acted as a negative control and received normal saline. Groups
II and III were administered TQ orally at doses of 10 and 20 mg/kg b.wt., respectively, for 21 days. The four group received AA
(20 mg/kg b.wt.) for 14 days. The five and six groups were given TQ at either dose for 21 days, starting seven days before AA
supplementation (for 14 days). Acrylamide intoxication was associated with significant (p < 0.05) increases in serum levels of
liver injury biomarkers (alanine transferase, aspartate transferase, and alkaline phosphatase), renal function products (urea,
creatinine), DNA oxidative damage biomarker (8-oxo-2′-deoxyguanosine), and pro-inflammatory biomarkers (interleukin-1β,
interleukin-6, and tumor necrosis factor-α). Moreover, AA intoxication was associated with increased lipid peroxidation and
nitric oxide levels, while reduced glutathione concentration and activities of glutathione peroxidase, superoxide dismutase, and
catalase in the liver, kidney, and brain. TQ administration normalized AA-induced changes in most serum parameters and
enhanced the antioxidant capacity in the liver, kidney, and brain tissues in a dose-dependent manner. In conclusion, the current
experiment showed that TQ exerted protective and antioxidant activities against AA-induced toxicity in mice.