The effect of carnosine treatment on prooxidant–antioxidant balance in liver, heart and brain tissues of male aged rats

Abstract

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.

Effect of carnosine supplementation on apoptosis and irisin, total oxidant and antioxidants levels in the serum, liver and lung tissues in rats exposed to formaldehyde inhalation

“…Several reports show that supplementation with other exogenous antioxidants, e.g. melatonin and carnosine, could eradicate the harmful effects of FA [2,47]. The total oxidant capacity increased with FA exposure in a dose-dependent way (low to high dose FA) in our study.…”

“…Several studies have reported decreased antioxidant capacity after FA exposure [6,19,20,39,[47][48][49]. We maintain that the decrease in antioxidant capacity associated with FA inhalation results from changes in the activities of antioxidant enzymes, such as glutathione reductase (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase [6, 19, 20, 39, , 47-49], as well as carnosine supplementation [2]. Carnosine and these enzymes adjust their activities to Page 13 of 29 A c c e p t e d M a n u s c r i p t 13 protect cells against oxidative damage [2,8].…”

“…We maintain that the decrease in antioxidant capacity associated with FA inhalation results from changes in the activities of antioxidant enzymes, such as glutathione reductase (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase [6, 19, 20, 39, , 47-49], as well as carnosine supplementation [2]. Carnosine and these enzymes adjust their activities to Page 13 of 29 A c c e p t e d M a n u s c r i p t 13 protect cells against oxidative damage [2,8]. Lino-dos-Santos-Franco et al reported that FA inhalation did not modify the activities of the activities of the glutathione reductase (GSH) and glutathione peroxidase (GSH-Px), but increase in superoxide dismutase and catalase in lung tissues [24].…”

“…Carnosine (C), an antioxidant dipeptide, beta-alanyl-L-histidine, is found in muscle and brain tissues [11]. It scavenges reactive oxygen radicals, hinders the oxidation of the cell membrane [2,11] and prevents diabetic nephropathy [32]. Carnosine prevents the development of cancers, protects against the oxidative stress caused by alcohol [11], and eliminates the hepatic injury associated with ethanol in animal models [7].…”

049 Physiological and molecular mechanisms associated with performance, immunometabolic status, and liver function in transition dairy cows fed rumen-protected methionine or choline

“…The fact that supplementation of carnosine in nonruminants was able to rescue prooxidant-antioxidant balance by restoring depleted levels of blood GSH and activities of antioxidant enzymes (Aydin et al, 2010) indicates the potential decrease in circulating carnosine in events of oxidative stress. Although the contribution of carnosine to restore prooxidant-antioxidant balance under physiologic (without carnosine supplementation) conditions remains unknown, the overall greater circulating carnosine together with greater circulating taurine as well as hepatic GSH reported previously (Zhou et al, 2016a) indicate a less pronounced oxidative stress status in response to periparturient MET supplementation.…”