Glutathione Reductase Activity In Tissues Research Articles

Interdependency of selected metabolic variables in an animal model of metabolic syndrome.

In the present study, the correlation between the percentage of glycated hemoglobin, taken as representative of changes in glucose homeostasis, and selected variables was investigated. Rats were treated for 8 weeks with diets containing 64% starch and 5% sunflower oil or containing 64% D-fructose mixed with: 5% sunflower oil; 3.4% sunflower oil and 1.6% salmon oil; or 3.4% sunflower oil and 1.6% safflower oil. Positive correlations were found between glycated hemoglobin and plasma albumin, urea, creatinine, phospholipids, triglycerides and total cholesterol, liver cholesterol, triglyceride and phospholipid content, and the plasma, liver, heart, kidney, soleus muscle and visceral adipose tissue content of thiobarbituric acid reactive substances, carbonyl derivatives and hydroperoxides. Inversely, negative correlations were observed between glycated hemoglobin and plasma calcium, iron and HDL-cholesterol concentrations, liver, heart, kidney, soleus muscle and visceral adipose tissue superoxide dismutase and catalase activity; as well as plasma, liver, heart, kidney, soleus muscle and visceral adipose tissue nitric oxide content. Only the liver glucokinase activity and liver, heart, kidney, soleus muscle and visceral adipose tissue glutathione reductase activity failed to display a significant correlation with glycated hemoglobin. These findings confirm the hypothesis that there is a close association between glucose homeostasis and other variables when considering the effects of long-chain polyunsaturated ω3 and ω6 fatty acids in rats with fructose-induced metabolic syndrome.

Antioxidant Defense System in Tadpoles of the American Bullfrog (Lithobates catesbeianus) Exposed to Paraquat

Abstract There is a great need for proactive approaches to avoid amphibian declines. We investigated the possibility that antioxidant stress markers might serve as a proactive measure of physiological stress in anuran tadpoles. Commercially purchased American Bullfrog tadpoles (Lithobates catesbeianus, Gosner stage 36–37) were subjected to 0- (control), 0.1-, 0.5-, 1.0-, and 2.0-mg/L paraquat for 24 h. Liver and muscle (tail clip) tissues were removed and analyzed for catalase, superoxide dismutase (SOD), general peroxidase, and glutathione reductase (GR) activities. In the controls, there was no significant difference in GR activity in tissues collected from the liver and the tail; however, peroxidase, SOD, and catalase activities ranged from two- to 20-fold higher in the liver than in the muscle tissue. Treatment with paraquat resulted in significant increases in SOD, general peroxidase, and GR activities in the liver tissue, whereas the high constitutively expressed catalase activity remained unchanged...

Oxidant/antioxidant status in liver tissue of vitamin B 6 deficient rats

The aim of this study was to evaluate the lipid peroxidation and antioxidant function in liver tissue of vitamin B6 deficient rats and investigate relationship among these parameters in either group. Twenty-four male rats with a weight of 48-59 g were used for the experiment. The rats were divided into control (n=12) and vitamin B6 deficient groups. After 4 weeks of feeding, the rats were killed by cervical dislocation and liver tissues were removed. Biochemical measurements in liver tissue were carried out using a spectrophotometer. Liver tissue antioxidant potential, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, total (enzymatic plus non-enzymatic) superoxide scavenger activity, non-enzymatic superoxide scavenger activity, glutathione levels were significantly lower in vitamin B6 deficient rats than in control group. However, liver tissue glutathione reductase activity, and MDA values were significantly higher in vitamin B6 deficient rats than in control group. These results explicitly indicate that vitamin B6 deficiency causes a decrease in antioxidant defense system and an increase in oxidant stress in liver tissue in rats.

Oxidative stress and inflammation contribute to lung toxicity after a common breast cancer chemotherapy regimen

Delayed pulmonary toxicity syndrome after high-dose chemotherapy (HDC) and autologous hematopoietic support occurs in up to 64% of women with advanced-stage breast cancer. Using a similar, but nonmyeloablative, HDC treatment regimen in mice, we found both immediate and persistent lung injury, coincident with marked decreases in lung tissue glutathione reductase activity and accompanied by increases in lung oxidized glutathione, bronchoalveolar lavage (BAL) lipid peroxidation, and BAL total cell counts. Most interestingly, at 6 wk, BAL total cell counts had increased fourfold, with lymphocyte cell counts increasing >11-fold. A single supplemental dose of glutathione prevented early lung injury at 48 h but showed no lung-protective effects at 6 wk, whereas single doses of other thiol-sparing agents (Ethyol and glutathione monoethyl ester) showed no benefit. These data suggest that this HDC regimen results in acute and persistent lung toxicity, induced in part by oxidative stress, that culminates with an acute lung cellular inflammatory response. Continuous glutathione supplementation and/or attenuation of the delayed pulmonary inflammatory response may prove beneficial in preventing lung toxicity after the use of these chemotherapeutic agents.

BCNU-induced protection from hyperbaric hyperoxia: role of glutathione metabolism.

To explore the role of the glutathione oxidation-reduction cycle in altering the sensitivity of rats to the effects of hyperbaric hyperoxia, we administered N,N-bis(2-chloroethyl)-N-nitrosourea (BCNU) to decrease tissue glutathione reductase activity. We then exposed these animals and their matched vehicle-treated controls to 100% O2 at 4 ATA. Animals that received BCNU and were immediately exposed to hyperbaric O2 showed enhanced toxicity by seizing earlier in the exposure than controls. Animals that received BCNU 18 h before the hyperbaric O2 exposure were paradoxically protected from the effects of the exposure with a prolongation of their time to initial seizure and a marked increase in their survival time during the exposure. Tissue glutathione concentrations were also measured in the various groups and the hyperbaric O2 exposure produced marked decreases in hepatic glutathione levels in all control animals. In animals treated with BCNU 18 h before exposure, hepatic glutathione concentrations also decreased, but the concentrations had significantly increased during the 18-h waiting period, allowing these animals to maintain hepatic levels in the normal range even during their hyperbaric exposures. We conclude that treatment of rats with BCNU 18 h before exposure to hyperbaric hyperoxia results in enhanced protection of the animals during the exposure.

Reduced and oxidised glutathione and glutathione-reductase activity in tissues of Pisum sativum

In three-week-old pea plants (Pisum sativum L., cv. Little Marvel) grown in the light, total glutathione levels were highest in apex and expanding leaves (1.5 μmol·(g FW)(-1)), and lower (0.4-0.6 μmol·(g FW)(-1)) in older leaves and roots. In the light period, levels in expanded leaves increased by about 40%, compared with dark values, with lesser increases in roots and apex. In illuminated plants the proportion in the reduced form was 86-88% in leaves and 80% in roots, and these values fell during the dark period (to 82% and 69%, respectively). Reduced glutathione makes up 65-70% of the low-molecular-weight thiol in leaves, but over 95% in roots. Chloroplasts contained about 10% of the leaf glutathione, at a concentration of 1-2 mM; total glutathione in the chloroplasts, and the proportion of oxidised form (GSSG) increased in light, while NADP(+)/NADPH ratios decreased, indicating both synthesis and active oxidation of glutathione in light. Chloroplasts contained 52% (young leaf) to 75% (mature leaf) of the GSSG-reductase (EC 1.6.4.2) activity in the leaves. In roots, over 30% of the GSSG reductase was in the plastid fraction. Very little GSSG-reductase activity was associated with mitochondria in leaf or root.

The effect of bcnu (carmustine) on tissue glutathione reductase activity

A single, 50 mg/kg i.p. dose of 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) to mice significantly inhibited glutathione reductase activity in liver within 10 min, and in lung and heart within 30 min. Maximal inhibition was reached at 4 h in all tissues and glutathione reductase activity remained significantly depressed for 48 h in liver and for 96 h in lung and heart. BCNU doses of less than 25 mg/kg had no effect on glutathione reductase activity. Increasing the BCNU dose to 100 mg/kg caused greater inhibition of glutathione reductase activity in all tissues. In spite of significantly decreased glutathione reductase activity, reduced glutathione (GSH) levels were unaffected in all tissues both 1 and 24 h after 50 mg/kg BNCU. These results suggest that lower than normal glutathione reductase activity is sufficient to maintain GSH levels. These results also demonstrate that BCNU inhibits tissue glutathione reductase activity for several days, but only at doses significantly greater than previously reported.