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Biomedical subjects

A Seven

Publications and source records attributed to A Seven.

At least 19 recordsLinked to original sources

Oxidative stress in heart tissue of hyperthyroid and iron supplemented rats.

This study was designed to investigate the effect of hyperthyroidism and/or iron supplementation or cardiac oxidative stress parameters--the lipid peroxidation end product glutathione (GSH), glutathione peroxidase (CSH-Px), and superoxide dismutase (CuZnSOD)--in rats. In plasma, ferritin as an indicator of iron status and glutamate oxaloacetate transaminase (GOT) as an indicator of damage to the heart tissue were analyzed. Our findings show that hyperthyroidism increased lipooxidative damage as reflected by higher lipid peroxidation end product levels and elevated antioxidant defense parameters-GSH and GSH-Px. Iron supplementation per se does not affect oxidative stress parameters studied in the euthyroid state. Although iron increased lipid peroxidation in the hyperthyroid state, this effect was less than that seen in euthyroidism. Iron supplementation to hyperthyroid rats significantly lowered plasma ferritin levels, suggesting increased iron elimination with consequently reduced oxidative stress.

Animals↗

Influence of propylthiouracil treatment on oxidative stress and nitric oxide in Basedow disease patients.

Oxidative stress parameters and nitric oxide (NO) values were determined in 27 newly diagnosed Basedow patients before and after 1 mo of propylthiouracil (PTU) therapy and in 15 healthy controls. Basedow patients exhibited increased triiodothyronine (T3) and thyroxine (T4) and decreased thyroid-stimulating hormone (TSH) values compared to controls. Significantly higher thiobarbituric acid-reactive substances (TBARS), NO and glutathione (GSH) levels, and CuZn superoxide dismutase (CuZn SOD) activity were found in Basedow patients in comparison to controls, regardless of sex. Treatment with PTU (3 x 100 mg/d for 30 d) was effective in decreasing T1 and T4 and increasing TSH levels. Significantly decreased NO and TBARS and increased GSH and CuZn SOD levels were observed in PTU-treated Basedow patients compared to pre-PTU administration. PTU-treated patients compared to controls still exhibited significantly higher T3 and lower TSH values and higher NO, TBARS, GSH, and CuZn SOD levels. The induced antioxidant defense and decrease in NO) values in response to PTU therapy emphasizes the role of PTU as an antithyroid drug, where the ability to diminish hyperthyroidism results in decreased catabolism and lower oxidant generation.

Adult↗

Biochemical evaluation of oxidative stress during exercise in patients with coronary heart disease.

The impact of exercise tolerance test on oxidative stress was assessed by thiobarbituric acid reactive substances and markers of antioxidant status, namely Cu Zn superoxide dismutase, glutathione peroxidase, glutathione and vitamin E in blood samples of patients with exertional angina. The study was aimed to differentiate patients with positive exercise test (coronary heart disease patients) from patients with negative exercise test, at rest and peak exercise with respect to the investigated variables. Significantly lower values for both glutathione peroxidase activity and glutathione level were observed in patients after exercise test (p<0.01 and p<0.05, respectively). Only the patients with positive exercise test had significantly lower values for Cu Zn superoxide dismutase, glutathione peroxidase and glutathione, and a significantly higher ratio of thiobarbituric acid reactive substances/glutathione after exercise, as compared to before (p<0.05, p<0.05, p<0.05, p<0.01, respectively). Our findings indicate that the exercise test applied to patients with exertional angina oxidatively stresses the erythrocytes to a greater extent in exercise test (+) patients than in exercise test (-) patients.

Adult↗

Evaluation of oxidative stress in experimental colitis: effects of L-arginine-nitric oxide pathway manipulation.

In this study it was of interest to evaluate the impact of nitric oxide (NO) modulation by administration of arginine/NAME, on oxidative stress in experimental colitis induced by 2,4,6-trinitrobenzenesulfonic acid. Arginine was used to increase NO levels while NAME lowered oxidant levels. Histopathological findings of colon revealed mucosal inflammation in all groups but significantly higher with arginine alone. The levels of NO and of thiobarbituric acid-reactive substances (TBARS, a marker of lipid peroxidation) were observed to be significantly higher in the arginine-administered group compared to glycine, and these levels were found to decrease on administration of NAME to both glycine- and L-arginine-administered groups. Glutathione peroxidase (GSH-Px) activity and glutathione (GSH) levels were significantly higher in arginine administered group compared to glycine. Significantly higher CuZn superoxide dismutase (CuZn-SOD) activity was observed in the L-arginine + L-NAME group compared to arginine. Data show that NO plays a role in oxidant damage found in experimental colitis and that the use of NAME may potentially inhibit injury.

Analysis of Variance↗

Comparison of oxidative stress indicators in plasma of recent-onset and long-term type 1 diabetic patients.

Oxidative stress was compared in plasma of 15 recently diagnosed (<2 mo) or 15 longstanding (>5 yr) type 1 diabetic patients with 15 healthy volunteers. Lipid peroxidation indices measured in plasma included thiobarbituric acid-reactive substances (TBARS), conjugated dienes, and lipid hydroperoxide (ROOH). The values obtained were corrected for phospholipid to minimize this as a confounding factor. In recently diagnosed diabetics, plasma conjugated lipid dienes were significantly elevated. However, in longstanding diabetics there was a marked increase in TBARS, conjugated dienes, and lipid hydroperoxide levels. Our findings showed increased oxidative stress in type 1 diabetics regardless of metabolic control and that conjugated diene measurement appeared to be the most sensitive bioindicator of oxidant stress in our population.

Adult↗

Evaluation of oxidative stress parameters in blood of patients with laryngeal carcinoma.

OBJECTIVES: In this study, plasma lipid peroxidation as assessed by thiobarbituric acid reactive substances and erythrocyte antioxidant status markers namely CuZn superoxide dismutase, glutathione peroxidase, glutathione and plasma levels of vitamin C and E were investigated in 20 patients with larygneal carcinoma and 15 healthy controls. DESIGN AND METHODS: Lipid peroxidation was observed to be significantly higher (0.01 > p > 0.001) in the larynx carcinoma group in comparison to the healthy controls. Both stage I + 11 and stage III carcinoma patients were observed to have significantly higher thiobarbituric acid reactive substances than the control group. A significant difference was found in plasma vitamin E level between the control group and stage I + 11 and stage III carcinoma patients (p < 0.01, 0.05 > p > 0.02, respectively). RESULTS: Our findings reveal the presence of increased lipooxidative damage in laryngeal carcinoma patients, but no change with respect to the endogenous antioxidant components-GSH, GSH Px, and CuZn SOD.

Adult↗

Lipid peroxidation and antioxidant state after laparoscopic and open cholecystectomy.

OBJECTIVE: To measure the amount of lipid peroxidation and erythrocyte antioxidation in patients undergoing laparoscopic and open cholecystectomy and healthy controls. DESIGN: Non-randomised study. SETTING: University hospital, Istanbul. SUBJECTS: 31 patients, of whom 14 underwent open and 17 laparoscopic cholecystectomy, and 15 healthy controls. INTERVENTIONS: Heparinised blood samples were taken from the patients immediately after operation and from the healthy controls. MAIN OUTCOME MEASURES: Lipid peroxidation index as expressed by thiobarbituric-acid-reactive substances (TBARS) and components of the erythrocyte antioxidant defence system, namely reduced glutathione, reduced glutathione peroxidase (glutathione-Px) and CuZn superoxide dismutase (CuZn SOD) in patients undergoing open or laparoscopic cholecystectomy and healthy controls. RESULTS: All 4 variables were significantly higher in the cholecystectomy groups than in controls (p < 0.001), and laparoscopic cholecystectomy caused significantly less oxidative stress than the open operation (p < 0.001). CONCLUSION: Both types of cholecystectomy cause oxidative stress and lead to an adaptive antioxidant response in the body. However; both oxidative stress and the antioxidant response are more pronounced after traditional open cholecystectomy.

Case-Control Studies↗

Evaluation of antioxidant status in liver tissues: effect of iron supplementation in experimental hyperthyroidism.

The antioxidant defense system in liver tissue in experimental hyperthyroidism and/or in iron supplementation was investigated. Thyroid hormones (T3, T4, TSH), ferritin (marker of iron status), antioxidant status components (glutathione [GSH], glutathione peroxidase [GSH-Px], superoxide dismutase [SOD]), and serum transaminases (GOT and GPT, both of which are known to be released from damaged hepatocytes), were measured. Hyperthyroidism in rats, induced by L-thyroxine administration, significantly raised SOD activity (p < 0.05), but significantly decreased GSH-Px activity and GSH values (p < 0.001) in the liver. In the L-thyroxine administered and iron supplemented (TI) group, GSH and GSH-Px values of liver tissues were significantly lower than those of control rats (p < 0.05). GSH-Px levels of the TI group were higher (p < 0.001), and SOD levels significantly lower (p < 0.001) than those of the L-thyroxine administered group. We conclude that hyperthyroidism induces SOD activity in liver; ferritin levels increase in hyperthyroidism, contributing to the antioxidant defense system; GSH-Px and GSH levels are decreased significantly in hyperthyroidism either due to inactivation due to increased oxidative stress or to insufficient synthesis; iron supple- and GPT analysis); iron decreases the effect of T4. This must be taken into consideration during iron supplementation.

Animals↗

The impact of propylthiouracil therapy on lipid peroxidation and antioxidant status parameters in hyperthyroid patients.

This study was performed on 17 hyperthyroid patients and 15 healthy controls. The patients were under propylthiouracil (PTU) therapy at a dosage of 3 x 100 mg/day for one month. Blood samples, taken at the beginning and on the 30th day of therapy, were analyzed for hormonal parameters (T3, T4, TSH), lipid peroxidation endproduct [thiobarbituric acid reactive substances (TBARS)] and antioxidant status parameters: glutathione (GSH), glutathione peroxidase (GSH-Px) and CuZn superoxide dismutase (CuZn SOD). Hyperthyroid patients were observed to have significantly higher TBARS, GSH and CuZn SOD levels than controls (P < 0.05, P < 0.001, P < 0.001, respectively). PTU therapy caused a relief in oxidative stress as reflected by significantly decreased TBARS levels (P < 0.001) and a selective modification in the antioxidant status parameters: significant decreases in GSH and CuZn SOD levels (P < 0.001) and a significant increase in GSH Px (P < 0.01) activity. Our findings suggest a selective modification of the antioxidative profile in hyperthyroidism. PTU should also be considered as an in vivo antioxidant, in addition to its antithyroid action.

Adult↗

Biochemical evaluation of oxidative stress in propylthiouracil treated hyperthyroid patients. Effects of vitamin C supplementation.

In this study the impact of vitamin C supplementation on oxidative damage as assessed by thiobarbituric acid reactive substances and markers of antioxidant status: namely Cu/Zn superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione were investigated in 24 hyperthyroid patients under propylthiouracil therapy (3x100 mg/day) for five days and in 15 healthy controls. Ascorbic acid (1000 mg/day) was given as a supplement for 1 month to both the patients and controls during the study period. Heparinised blood samples were taken at the beginning and the end of one month ascorbic acid supplementation. Comparison of the hyperthyroid patients with the controls revealed higher lipid peroxidation (p<0.001), higher Cu/Zn superoxide dismutase activity (p<0.001), higher glutathione level (p<0.001) and lower glutathione reductase activity (p<0.001). Vitamin C supplementation to hyperthyroid patients caused significant increases in glutathione concentration (p<0.001) and glutathione peroxidase activity (p<0.001), whereas there were significant decreases in glutathione reductase (p<0.001) and Cu/Zn superoxide dismutase activities (p<0.01). Thiobarbituric acid reactive substances and thiobarbituric acid reactive substances/glutathione ratio were significantly decreased (p<0.01). Vitamin C supplementation to euthyroid controls caused significant increases in glutathione concentration (p<0.001) and glutathione peroxidase and Cu/Zn superoxide dismutase activities (p<0.001), whereas there was a significant decrease in glutathione reductase (p<0.001). The thiobarbituric acid reactive substances/glutathione ratio was significantly decreased (p<0.05). Our findings reveal the potentiation of antioxidant status and a relief in oxidative stress in both propylthiouracil treated hyperthyroid patients and controls in response to vitamin C supplementation.

Adult↗

Breast cancer and benign breast disease patients evaluated in relation to oxidative stress.

In this study, breast cancer (n = 23) and benign breast disease (n = 15) patients were evaluated in relation to oxidative stress. The extent of lipid peroxidation was assessed by measuring thiobarbituric acid reactive substances (TBARS) in plasma. Erythrocyte glutathione peroxidase (GSH Px), CuZn speroxide dismutase (CuZn SOD), glutathione (GSH) and plasma vitamin E, cholesterol Fe, Zn, Cu levels were analysed in both groups GSH Px (p < 0.01), vitamin E (p < 0.001), Zn (p < 0.01), Cu (p < 0.05) and cholesterol (p < 0.01) concentrations were found to be significantly increased, TBARS level (p < 0.01) significantly decreased in breast cancer patients in comparison to benign breast disease group.

Breast Diseases↗

Lipid peroxidation and antioxidant status in experimental animals: effects of aging and hypercholesterolemic diet.

Effects of aging and hypercholesterolemic diet on lipid peroxidation and antioxidant status were investigated in rats. The rats were divided into four groups of ten: Group I; young rats receiving standard lab chow; Group II; young rats on hypercholesterolemic diet (0.4 g/rat/day); Group III; aged rates receiving standard lab chow; Group IV; aged rats on hypercholesterolemic diet (0.4 g/rat/day). Plasma lipid peroxidation end product level was determined as thiobarbutiric acid reactive substances (TBARS). Plasma cholesterol concentration was analyzed by a kinetic enzymatic method. Erythrocyte superoxide dismutase (CuZn SOD), glutathione peroxidase (GSH Px) and glutathione (GSH) levels were determined spectrophotometrically. Cholesterol values were found to be significantly high (p < 0.001), TBARS (0.05 > p > 0.02) and GSH (p < 0.001) levels significantly low in aged rats in comparison with young rats. Hypercholesterolemic diet induced significant increases in GSH (p < 0.001) and CuZn SOD (p < 0.001) levels, whereas a significant decrease in GSH Px activity (0.05 > p > 0.02) was observed in aged rats. In young rats hypercholesterolemic diet caused a significant increase in both GSH and CuZnSOD levels. Our results indicate an imbalance between radical production and destruction in favour of prooxidant conditions in the young rats and the induction by hypercholesterolemic diet of the antioxidative response in erythrocytes.

Aging↗

Could L-carnitine be an acute energy inducer in catabolic conditions?

Serum free carnitine levels in five children (aged between 2.5 months and 4 years) with the findings of septic shock without disseminated intravascular coagulopathy and seven children (aged between 1.5 and 6.5 years) with the first attack of idiopathic status epilepticus were compared with those of eight healthy children (aged between 2.5 months and 5 years). Serum free carnitine levels showed a statistically significant decrease in the sepsis (mean 51.5 +/- 19 mg/L) and status epilepticus groups (mean 4.1 +/- 12.4 mg/L) (P = 0.006 and P = 0.001, respectively) when compared with the controls (mean 90.8 +/- 17.2 mg/L).

Carnitine↗

The effect of iron supplementation on GSH levels, GSH-Px, and SOD activities of erythrocytes in L-thyroxine administration.

Our aim was to study the effect of iron supplementation on the following aspects of erythrocyte metabolism in experimental hyperthyroidism: glutathione (GSH) levels, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities. Hyperthyroidism induced by L-thyroxine administrations significantly raised erythrocyte GSH, GSH-Px and SOD levels of the rats (P < 0.001). Likewise, we observed that iron supplementation induced significant rises in erythrocyte GSH, GSH-Px and SOD levels (P < 0.001) as compared with the control group. The erythrocyte GSH, GSH-Px and SOD levels of hyperthyroidism-induced iron-supplemented animals were significantly higher when compared with either the iron-supplemented group (P < 0.001) or the only L-thyroxine-administered hyperthyroid group (P < 0.001, P < 0.05, P < 0.01, respectively). The results of this study show that L-thyroxine administration and/or iron supplementation increases GSH, GSH-Px and SOD levels of erythrocytes.

Animals↗

Antioxidant status in experimental hyperthyroidism: effect of vitamin E supplementation.

Free radical-mediated oxidative stress has been implicated in the genesis and exacerbation of degenerative diseases. In view of the role of oxidative processes in hyperthyroidism, in this study, we investigated the antioxidant status of erythrocytes in experimental hyperthyroidism and the effect of vitamin E supplementation on defense systems. Our findings of significantly increased T4 and T3 and undetectable TSH values in thyroxine administered rats confirmed the establishment of hyperthyroidism. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) values were found to be significantly increased in hyperthyroid rats in comparison to the control group. Vitamin E supplementation to hyperthyroid rats induced a significant decrease in GSH-Px activity and a significant increase in GSH level. These findings show that hyperthyroidism increases the components of the antioxidant system in the erythrocytes. Furthermore, vitamin E supplementation reduces the burden of oxidative stress in hyperthyroidism.

Animals↗