Protective effects of thymoquinone against acrylamide-induced liver, kidney and brain oxidative damage in rats

• Published in: Environmental science and pollution research international Vol. 27; no. 30; pp. 37709 - 37717
• Main Authors: Abdel-Daim, Mohamed M., Abo El-Ela, Fatma I., Alshahrani, Fatima K., Bin-Jumah, May, Al-Zharani, Mohammed, Almutairi, Bader, Alyousif, Mohamed S., Bungau, Simona, Aleya, Lotfi, Alkahtani, Saad
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.10.2020; Springer Nature B.V; Springer Verlag
• Subjects: Acrylamide; Alanine; Alkaline phosphatase; Antioxidants; Aquatic Pollution; Atmospheric Protection/Air Quality Control/Air Pollution; Biomarkers; Brain; Brain damage; Brain injury; Catalase; Creatinine; Cytokines; Deoxyguanosine; DNA damage; Earth and Environmental Science; Ecotoxicology; Environment; Environmental Chemistry; Environmental Health; Environmental science; Environmental Sciences; Glutathione; Glutathione peroxidase; Inflammation; Interleukin 6; Interleukins; Intoxication; Kidneys; Lipid peroxidation; Lipids; Liver; Nitric oxide; Oxidation; Oxidative stress; Peroxidase; Peroxidation; Renal function; Research Article; Serum levels; Superoxide dismutase; Supplements; Toxicity; Tumor necrosis factor-α; Urea; Waste Water Technology; Water Management; Water Pollution Control; Acrylamide; Neurotoxicity; Antioxidant; Hepatotoxicity; Nephrotoxicity; Thymoquinone; Acrylamide . Thymoquinone . Antioxidant . Hepatotoxicity . Nephrotoxicity . Neurotoxicity
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-020-09516-3

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.