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Carnosine (beta-alanyl-L: -histidine) is a dipeptide with antioxidant properties. Oxidative damage by free radicals is one of the mechanisms underlying the aging process. This study was done to investigate the effects of carnosine treatment on lipid peroxidation and antioxidant status of liver, heart, brain in male young and aged rats. At the initiation of study, young and aged rats were 5 and 22 months old, respectively. Carnosine (250 mg/kg, daily, i.p.) was administered for 1 month to rats. At the end of this period, malondialdehyde (MDA) and diene conjugate (DC) and protein carbonyl (PC) levels, glutathione (GSH), vitamin E and vitamin C levels and Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities were determined in tissues of carnosine-treated young and old rats. Liver and heart, but not brain MDA and DC levels increased significantly in aged rats as compared to young rats. Liver PC levels were also significantly elevated. Significant decreases in GSH and vitamin C levels and SOD activities were detected in liver of aged rats, but vitamin E levels and GSH-Px and GST activities remained unchanged. Non-enzymatic and enzymatic antioxidants did not change in heart and brain of aged rats. Carnosine treatment decreased high MDA, DC and PC levels and caused significant increases in vitamin E level and SOD activity in the liver of aged rats. There were no changes in non-enzymatic and enzymatic antioxidants in the heart and brain of carnosine-treated aged rats. In conclusion, carnosine treatment was found to be useful in the decrease of age-related oxidative stress in the liver.

Hypercholesterolemia and lipid peroxidation play complementary roles in atherosclerosis. Artichoke (Cynara scolymus L., Asteraceae) leaf extract (ALE), rich in antioxidants, has cholesterol-reducing effect. We investigated the effect of ALE on serum and hepatic lipid levels and pro-oxidant-antioxidant balance in the liver and heart of hypercholesterolemic rats. Rats were fed on 4% (w/w) cholesterol and 1% cholic acid (w/w) supplemented diet for 1 month. ALE (1.5 g/kg/day) was given by gavage during the last 2 weeks. High cholesterol (HC) diet caused significant increases in serum and liver cholesterol and triglyceride levels. It increased malondialdehyde (MDA) and diene conjugate (DC) levels in both tissues. Hepatic vitamin E levels and hepatic and cardiac glutathione peroxidase (GSH-Px) activities decreased, but superoxide dismutase and glutathione transferase activities, glutathione, and vitamin C levels remained unchanged due to HC diet. Serum cholesterol and triglyceride levels and ratio of cholesterol to high-density lipoprotein (HDL)-cholesterol decreased in ALE plus HC-treated rats, but liver cholesterol and triglyceride levels remained unchanged. Significant decreases in hepatic and cardiac MDA and DC levels and increases in hepatic vitamin E and GSH-Px activities were observed in ALE-treated hypercholesterolemic rats. Our results indicate that ALE decreases serum lipids and hypercholesterolemia-induced pro-oxidant state in both tissues.

Objective• To evaluate the relationship between manganese superoxide dismutase (MnSOD) Ile58Thr, catalase (CAT) C-262T and myeloperoxidase (MPO) G-463A gene polymorphisms and the susceptibility and clinicopathological characteristics of prostate cancer. Patients and Methods• In all, 155 patients diagnosed with prostate cancer and 195 controls with negative digital rectal examinations and PSA levels of <4 ng/dL were enrolled in this study.• MnSOD, CAT and MPO gene polymorphisms were identified by polymerase chain reaction restriction-fragment length polymorphism methods.

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High-fat diet (HFD) and low-dose streptozotocin (STZ)-treated rats provide useful animal model for type II diabetes mellitus. Oxidative stress and advanced glycation end products (AGEs) play a role in the development of diabetic complications. Carnosine (CAR) has anti-oxidant and anti-glycating properties. We investigated the effects of CAR on oxidation and glycation products in HFD+STZ rats. Rats were fed with HFD (60% of total calories from fat) for 4 weeks, and then a single dose of STZ (40 mg/kg; i.p.) was applied. Rats with blood glucose levels above 200 mg/dl were fed with HFD until the end of the 12th week. CAR (250 mg/kg body weight; i.p.; five times a week) was administered to the rats for the last four weeks. CAR significantly decreased serum triglyceride (TG) (57.7%), cholesterol (35.6%) levels and hepatic marker enzyme activities of HFD+STZ rats. It significantly reduced serum reactive oxygen species (ROS) (23.7%), AGEs (13.4%) and advanced oxidized protein products (AOPP) (35.9%) and hepatic TG (59%), ROS (26%), malondialdehyde (MDA) (11.5%), protein carbonyl (PC) (19.2%) and AGE (20.2%) levels. Liver steatosis and hepatocyte ballooning were also significantly reduced. However, CAR treatment did not alter serum glucose and blood glycated haemoglobin and hepatic anti-oxidant enzyme activities/mRNA expressions in HFD+STZ rats. Our results indicate that CAR decreased accumulation of oxidation and glycation products, such as MDA, AGE, AOPP and PC in the serum and liver and ameliorated hepatic dysfunction in HFD+STZ rats. This effect may be related to its anti-oxidative, anti-glycating, and anti-lipogenic potential.

This study was conducted to investigate the association of genetic polymorphisms in the MnSOD and GPX1 genes with the risk and invasiveness of bladder cancer in a Turkish population. This prospectively designed study enrolled 157 patients with bladder cancer (mean age 63.2 ± 10.86 years) and 224 healthy controls (mean age 61.7 ± 8.39 years). Genotyping of the MnSOD Ala-9Val and GPX1 Pro198Leu polymorphisms was carried out by PCR-RFLP. No significant difference was found in MnSOD genotype distributions between the controls and the bladder cancer patients. However, the Leu/Leu genotype of GPX1 was associated with a significantly higher risk of bladder cancer than the Pro/Pro genotype. When stratified according to tumor stage, the Leu/Leu genotype of GPX1 was more frequently observed in bladder cancer patients with high-stage tumors than those with low-stage tumors. Additionally, patients carrying both Ala/Ala of MnSOD and Leu/Leu of GPX1 had the highest risk of developing bladder cancer. In conclusion, the present study indicates that the GPX1 Pro198Leu polymorphism may be associated with the risk and development of invasive bladder cancer. In addition, the combination of the MnSOD Ala/Ala and GPX1 Leu/Leu genotypes may have a synergistic effect on disease risk.

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