31 research outputs found
The endothelin 1 and endothelin receptor A gene polymorphisms increase the risk of developing papillary thyroid cancer.
N-Acetylcysteine supplementation decreased brain lipid and protein oxidations produced by experimental homocysteine thiolactone exposure: Relevance to neurodegeneration.
Association of Leukotrichia in Vitiligo and Asp148Glu Polymorphism of Apurinic/Apyrimidinic Endonuclease 1.
2-(5-R-1H-benzimidazol-2-yl)-4-metil/bromo-fenoller ile bazı geçiş metal komplekslerinin yapılarının ve antibakteriyel etkilerinin incelemesi
α-Lipoic Acid Ameliorates The Changes in Prooxidant-Antioxidant Balance in Liver and Brain Tissues of Propylthiouracil-Induced Hypothyroid Rats.
Objective: There are controversial data about the prooxidant-antioxidant balance in hypothyroidism. We aimed to investigate the effect of alpha-lipoic acid (ALA) on oxidative stress parameters in the liver and brain of propylthiouracil (PTU)-induced hypothyroid rats
XRCC4 rs6869366 polymorphism is associated with suspectibility to nicotine dependence and/or schizophrenia
The effect of resveratrol on glycation and oxidation products in plasma and liver of chronic methylglyoxal-treated rats.
Ameliorative effect of carnosine and N‐acetylcysteine against sodium nitrite induced nephrotoxicity in rats
Effect of carnosine alone or combined with α-tocopherol on hepatic steatosis and oxidative stress in fructose-induced insulin-resistant rats
A diet high in fructose (HFr) induces insulin resistance in animals. Free radicals are involved in the pathogenesis of HFr-induced insulin resistance. Carnosine (CAR) is a dipeptide with antioxidant properties. We investigated the effect of CAR alone or in combination with a-tocopherol (CAR+TOC) on HFr-induced insulin-resistant rats. Rats fed with HFr containing 60 % fructose received CAR (2 g/L in drinking water) with/without TOC (200 mg/kg, i.m. twice a week) for 8 weeks. Insulin resistance, serum lipids, inflammation markers, hepatic lipids, lipid peroxides, and glutathione (GSH) levels together with glutathione peroxidase (GSH-Px) and superoxide dismutase 1 (CuZnSOD; SOD1) activities and their protein expressions were measured. Hepatic histopathological examinations were performed. HFr was observed to cause insulin resistance, inflammation and hypertriglyceridemia, and increased triglyceride and lipid peroxide levels in the liver. GSH-Px activity and expression decreased, but GSH levels and SOD1 activity and expression did not alter in HFr rats. Hepatic marker enzyme activities in serum increased and marked macro-and microvesicular steatosis were seen in the liver. CAR treatment did not alter insulin resistance and hypertriglyceridemia, but it decreased steatosis and lipid peroxidation without any change in the antioxidant system of the liver. However, CAR+TOC treatment decreased insulin resistance, inflammation, hepatic steatosis, and lipid peroxidation and increased GSH-Px activity and expression in the liver. Our results may indicate that CAR+ TOC treatment is more effective to decrease HFr-induced insulin resistance, inflammation, hepatic steatosis, and dysfunction and pro-oxidant status in rats than CAR alone