Biomedical subjects

Refik Kayali

Publications and source records attributed to Refik Kayali.

6 recordsLinked to original sources

PubMed2005

Plasma protein oxidation in aging rats after alpha-lipoic acid administration.

In the present study, we investigated whether alpha-lipoic acid administration could have prooxidant or antioxidant effect on oxidative protein damage parameters such as protein carbonyl, nitrotyrosine, advanced oxidation protein products, and protein thiol, as well as oxidative stress parameters such as total thiol, nonprotein thiol, and lipid hydroperoxide in the plasma proteins of aged rats. Alpha-lipoic acid (100 mg/kg body wt/day) was administrated intraperitoneally to the Sprague-Dawley rats for 14 days. Protein carbonyl, nitrotyrosine, and advanced oxidation protein products levels were increased, protein thiol, nonprotein thiol, and total thiol levels were not changed in the plasma proteins of aged rats with alpha-lipoic acid administration. In aging rats with and without alpha-lipoic acid administration, plasma lipid hydroperoxide levels were significantly increased compared with those of the control group. The increased levels of protein oxidation markers such as protein carbonyl, nitrotyrosine and advanced oxidation protein products in the plasma proteins of alpha-lipoic acid-administrated aged rats compared with nonadministrated aged rats suggests that protein oxidation is increased in alpha-lipoic acid-administrated aged rats. We assume that an explanation for our findings regarding alpha-lipoic acid administration on protein oxidation markers in the plasma proteins of aged rats may be due to the prooxidant effects of alpha-lipoic acid.

Aging↗

PubMed2003

Relation of aging with oxidative protein damage parameters in the rat skeletal muscle.

OBJECTIVES: An increase in oxidative stress may contribute to the development of oxidative protein damage in the aging rat skeletal muscle. Our aim was to reveal protein carbonyl (PCO), advanced oxidation protein products (AOPP), a novel marker of oxidative stress, and protein thiol (P-SH) levels as markers of protein oxidation, as well as lipid hydroperoxide (LHP) levels as a marker of lipid peroxidation, and relation of nitrotyrosine (NT) levels with these markers in skeletal muscle tissue of young, adult, and old male Wistar rats. DESIGN AND METHODS: In the present study, we investigated the relation between aging and oxidative protein damage parameters such as PCO, NT, AOPP, and P-SH, as well as oxidative stress parameters such as total thiol, nonprotein thiol, and LHP in the skeletal muscle tissue of young, adult, and old Wistar rats. RESULTS: PCO and NT levels of old rats were significantly increased compared with those of young and adult rats. Skeletal muscle AOPP levels were significantly increased in old rats compared with those of adult rats. P-SH levels were significantly decreased in old rats compared with those of young rats. CONCLUSIONS: The finding that the increase in PCO levels of young vs. old group was more significant than that of adult vs. old group may suggest that PCO formation is an early specific marker of aging process in skeletal muscle. In addition, increased levels of nitrotyrosine in the skeletal muscle of the old rat group may be a novel specific marker of oxidative protein damage in the aging muscle. The absence of correlation between oxidative protein damage markers mentioned above and LHP levels may indicate that protein oxidation and lipid peroxidation in the aging rat skeletal tissue are two distinct mechanisms.

Aging↗

PubMed2002

Effect of alpha-lipoic acid on lipid peroxidation and anti-oxidant enzyme activities in diabetic rats.

1. Oxidative damage has been suggested to be a contributory factor in the development and complications of diabetes. Recently, alpha-lipoic acid (ALA) has gained considerable interest as an anti-oxidant. Various studies have indicated the anti- oxidant effects of ALA and its reduced form dihydrolipoic acid. Therefore, it appears that these compounds have important therapeutic potential in conditions where oxidative stress is involved. The aim of the present study was to investigate the effect of ALA supplementation on lipid peroxidation and anti-oxidant enzyme activities in various tissues in diabetic rats. 2. Male Wistar rats were divided into three groups. Diabetes was induced by streptozotocin (STZ) injection in the two groups of rats to be supplemented and not to be supplemented with ALA. Another group of rats, which received saline injection, formed the control group. After 5 weeks of diabetes, rats were killed. In order to assess the redox status of various organs in the diabetic and control rats, thiobarbituric acid-reactive substances (TBARS) and glutathione (GSH) levels, as well as superoxide dismutase (SOD), glutathione peroxidase (G-Px) and glutathione reductase (G-Red) activities were determined in the liver, pancreas and kidney. 3. In both diabetic groups, TBARS levels and SOD activity were increased in the liver and pancreas, G-Px and G-Red activities were increased in the kidney and GSH levels were decreased in all organs compared with controls. In the ALA- supplemented group, TBARS levels were decreased, GSH levels were increased in the liver and pancreas, SOD activity was decreased in the liver, G-Px activity remained unchanged in all tissues and G-Red activity was increased in the pancreas compared with the diabetic group that did not receive ALA supplementation. 4. In conclusion, ALA supplementation has disparate effects on the redox status of different organs. These data are not sufficient for confirmation the beneficial effects of ALA supplementation on the redox status of various organs in diabetic rats.

Animals↗

PubMedDate not supplied

Effect of alpha-lipoic acid supplementation on markers of protein oxidation in post-mitotic tissues of ageing rat.

In the present study, we investigated whether DL-alpha-lipoic acid (LA) supplementation could have prooxidant or antioxidant effects on oxidative protein damage parameters such as protein carbonyl (PCO), nitrotyrosine (NT), advanced oxidation protein products (AOPP), and protein thiol (P-SH), as well as oxidative stress parameters such as total thiol (T-SH), non-protein thiol (Np-SH), and lipid hydroperoxide (LHP) in the brain and the skeletal muscle tissue of aged rats. PCO, and NT levels were increased, AOPP and P-SH levels were not changed in the brain tissue of aged rats given LA supplementation. On the other hand, TSH, Np-SH, and LHP levels were decreased in the brain tissue of aged rats given LA supplementation. The levels of the same parameters were not significantly different in the skeletal muscle tissue of aged rats given LA supplementation. The increased levels of protein oxidation markers such as PCO, and NT in the brain tissue of LA-supplemented aged rats compared with non-supplemented aged rats may suggest that oxidative protein damage is increased in LA-supplemented aged rats. We assume that an explanation for our findings regarding LA supplementation on protein oxidation markers in the brain tissue of aged rats may be due to the prooxidant effects of LA. Depending on post-mitotic tissue type and dosage of LA, the prooxidant effects of LA supplementation, should be considered in future studies.

Aging↗

PubMedDate not supplied

Decrease in mitochondrial oxidative protein damage parameters in the streptozotocin-diabetic rat.

BACKGROUND: Many authors have shown that hyperglycemia leads to an increase in oxidative protein damage in diabetes. The aim of this study was to reveal the susceptibility of mitochondria from liver, pancreas, kidney, and skeletal muscle of diabetic Sprague-Dawley rats, a model of type 1 diabetes, to oxidative protein damage. METHODS: Mitochondrial fractions were obtained by differential centrifugation. To show the effect of hyperglycemia in promoting oxidative protein damage, we determined mitochondrial protein carbonyl, total thiol, nitrotyrosine, advanced oxidation protein products, and lipid hydroperoxide levels. The levels of the studied markers, except nitrotyrosine, were determined by colorimetric methods. Nitrotyrosine levels were measured by ELISA. All values were compared with those of the controls by using the Mann-Whitney U-test. RESULTS: Nitrotyrosine and lipid hydroperoxide levels were decreased and other parameters were not changed in liver mitochondria of diabetic rats. Protein carbonyl, nitrotyrosine, advanced oxidation protein products, and lipid hydroperoxide levels were decreased and total thiol levels were not changed in pancreas mitochondria of diabetic rats. Only advanced oxidation protein products and lipid hydroperoxide levels were decreased in kidney mitochondria of diabetic rats. The levels of the same parameters were not significantly different in muscle mitochondria of diabetic rats. CONCLUSIONS: The decrease in mitochondrial oxidative protein damage in diabetes may correspond to either an increase in antioxidant defense mechanisms or a different adaptive response of the cells to the increased extramitochondrial oxidative stress in diabetes. The mitochondrial oxidative protein damage-lowering mechanisms in diabetes remain to be clarified.

Animals↗

PubMedDate not supplied

Prooxidant activities of alpha-lipoic acid on oxidative protein damage in the aging rat heart muscle.

In the present study, we investigated whether alpha-lipoic acid (ALA) supplementation could have prooxidant or antioxidant effects on protein oxidation parameters such as protein carbonyl (PCO), nitrotyrosine (NT), advanced oxidation protein products (AOPP), and protein thiol (P-SH), as well as oxidative stress parameters such as total thiol (T-SH), non-protein thiol (Np-SH), and lipid hydroperoxide (LHP) in the heart muscle tissue of aged rats. ALA (100 mg/kg body wt/day) was administered intraperitoneally to the experimental animals for 14 days. PCO, NT, AOPP, and P-SH levels were increased, T-SH and Np-SH levels were not changed, and only LHP levels were decreased in the heart muscle tissue of aged rats with ALA supplementation. When compared with non-supplemented aged rats, increasing levels of protein oxidation markers such as PCO, NT, and AOPP in ALA-supplemented aged rats may suggest that oxidative protein damage is increased in ALA-supplemented aged rats. We assume that an explanation for our findings regarding ALA supplementation on protein oxidation markers in the heart muscle tissue of aged rats may be due to the prooxidant effects of ALA. The prooxidant effects of ALA supplementation should be considered in future studies.

Animals↗