Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia.
Pharmacology Department, Faculty of Veterinary Medicine, Suez Canal University, Ismailia, 41522, Egypt.
Environ Sci Pollut Res Int. 2020 Oct;27(30):37709-37717. doi: 10.1007/s11356-020-09516-3. Epub 2020 Jun 30.
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.
丙烯酰胺（AA），一种工业单体，可能通过诱导氧化应激和炎症引起多器官毒性。先前已经证实，黑种草中一种活性成分——百里醌（TQ）具有抗氧化特性。本研究旨在评估 TQ 对大鼠 AA 诱导毒性的保护作用。48 只雄性 Wistar 大鼠被分为 6 组，每组 8 只。第一组作为阴性对照，给予生理盐水。第二组和第三组分别口服 TQ，剂量为 10 和 20mg/kg 体重，共 21 天。第四组给予 AA（20mg/kg 体重）14 天。第五组和第六组在开始 AA 补充前 7 天（共 14 天），以任一剂量给予 TQ 21 天。丙烯酰胺中毒与血清肝损伤生物标志物（丙氨酸转移酶、天冬氨酸转移酶和碱性磷酸酶）、肾功能产物（尿素、肌酐）、DNA 氧化损伤生物标志物（8-氧-2'-脱氧鸟苷）和促炎生物标志物（白细胞介素-1β、白细胞介素-6 和肿瘤坏死因子-α）水平显著升高有关（p<0.05）。此外，AA 中毒与肝、肾和脑中脂质过氧化和一氧化氮水平升高有关，而还原型谷胱甘肽浓度和谷胱甘肽过氧化物酶、超氧化物歧化酶和过氧化氢酶活性降低。TQ 给药使 AA 诱导的大多数血清参数变化正常化，并以剂量依赖的方式增强肝、肾和脑组织中的抗氧化能力。总之，本实验表明 TQ 对 AA 诱导的小鼠毒性具有保护和抗氧化作用。
