scholarly journals Antioxidant enzyme activities and markers of oxidative stress in the life cycle of earthworm,Eudrilus eugeniae

2010 ◽  
Vol 77 (2) ◽  
pp. 144-148 ◽  
Author(s):  
T. Ravi Kiran ◽  
H. K. Aruna
2007 ◽  
Vol 53 (3) ◽  
pp. 511-519 ◽  
Author(s):  
Jason HY Wu ◽  
Natalie C Ward ◽  
Adeline P Indrawan ◽  
Coral-Ann Almeida ◽  
Jonathan M Hodgson ◽  
...  

Abstract Background: Vitamin E isomers may protect against atherosclerosis. The aim of this study was to compare the effects of supplementation with either α-tocopherol (αT) or mixed tocopherols rich in γ-tocopherol (γT) on markers of oxidative stress and inflammation in patients with type 2 diabetes. Methods: In a double-blind, placebo-controlled trial, 55 patients with type 2 diabetes were randomly assigned to receive (500 mg/day) (a) αT, (b) mixed tocopherols, or (c) placebo for 6 weeks. Cellular tocopherols, plasma and urine F2-isoprostanes, erythrocyte antioxidant enzyme activities, plasma inflammatory markers, and ex vivo assessment of eicosanoid synthesis were analyzed pre- and postsupplementation. Results: Neutrophil αT and γT increased (both P <0.001) with mixed tocopherol supplementation, whereas αT (P <0.001) increased and γT decreased (P <0.005) after αT supplementation. Both αT and mixed tocopherol supplementation resulted in reduced plasma F2-isoprostanes (P <0.001 and P = 0.001, respectively) but did not affect 24-h urinary F2-isoprostanes or erythrocyte antioxidant enzyme activities. Neither αT nor mixed tocopherol supplementation affected plasma C-reactive protein, interleukin 6, tumor necrosis factor-α, or monocyte chemoattractant protein-1. Stimulated neutrophil leukotriene B4 production decreased significantly in the mixed tocopherol group (P = 0.02) but not in the αT group (P = 0.15). Conclusions: The ability of tocopherols to reduce systemic oxidative stress suggests potential benefits of vitamin E supplementation in patients with type 2 diabetes. In populations with well-controlled type 2 diabetes, supplementation with either αT or mixed tocopherols rich in γT is unlikely to confer further benefits in reducing inflammation.


2017 ◽  
Vol 117 (3) ◽  
pp. 335-350 ◽  
Author(s):  
Susmita Barman ◽  
Krishnapura Srinivasan

AbstractOxidative stress plays a major role in the pathogenesis of diabetes mellitus, which further exacerbates damage of cardiac, hepatic and other tissues. We have recently reported that Zn supplementation beneficially modulates hyperglycaemia and hypoinsulinaemia, with attendant reduction of associated metabolic abnormalities in diabetic rats. The present study assessed the potential of Zn supplementation in modulating oxidative stress and cardioprotective effects in diabetic rats. Diabetes was induced in Wistar rats with streptozotocin, and groups of diabetic rats were treated with 5- and 10-fold dietary Zn interventions (0·19 and 0·38 g Zn/kg diet) for 6 weeks. The markers of oxidative stress, antioxidant enzyme activities and concentrations of antioxidant molecules, lipid profile, and expressions of fibrosis and pro-apoptotic factors in the cardiac tissue were particularly assessed. Supplemental Zn showed significant attenuation of diabetes-induced oxidative stress in terms of altered antioxidant enzyme activities and increased the concentrations of antioxidant molecules. Hypercholesterolaemia and hyperlipidaemia were also significantly countered by Zn supplementation. Along with attenuated oxidative stress, Zn supplementation also showed significant cardioprotective effects by altering the mRNA expressions of fibrosis and pro-apoptotic factors (by >50 %). The expression of lipid oxidative marker 4-hydroxy-2-nonenal (4-HNE) protein in cardiac tissue of diabetic animals was rectified (68 %) by Zn supplementation. Elevated cardiac and hepatic markers in circulation and pathological abnormalities in cardiac and hepatic tissue architecture of diabetic animals were ameliorated by dietary Zn intervention. The present study indicates that Zn supplementation can attenuate diabetes-induced oxidative stress in circulation as well as in cardiac and hepatic tissues.


2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Mariusz Kozakiewicz ◽  
Rafał Rowiński ◽  
Maciej Kornatowski ◽  
Andrzej Dąbrowski ◽  
Kornelia Kędziora-Kornatowska ◽  
...  

The aim of the present study was to establish whether markers of oxidative stress and the enzymatic defense system of the blood are related to moderate physical activity in younger old and the oldest old men. They were divided into four groups according to the age and level of physical activity (groups YN and YA—inactive and active younger old men aged 65-74 years, groups ON and OA—inactive and active oldest old men aged 90-99 years). Venous blood was collected from the subjects in the morning before breakfast. MDA concentration and antioxidant enzyme activities (SOD, CAT, GPx, and GR) in erythrocyte hemolysates were assayed. The concentration of isoprostanes (8-iso-PGF2α) and carbonyl groups in protein (CP) was measured in plasma and serum. All assayed antioxidant enzyme activities and the SOD/GPx ratios were significantly higher in the active younger old males than in all the inactive ones. In the group of oldest old active participants, only the GPx activity was significantly higher compared to the inactive oldest old males. The activity of CAT and GPx in the younger old inactive men was significantly lower than that in the oldest old inactive subjects. However, SOD, CAT, and GR activities and SOD/GPx ratio were significantly higher in the younger old active men compared to the oldest old active participants. The concentrations of isoprostanes, protein carbonyls, and MDA were significantly lower in both active and inactive younger old males than in the respective groups of the oldest old men and in both groups of active men, independently of age, compared to the respective inactive subjects. The present study confirmed that oxidative stress is related to age. Physical activity caused a decrease of oxidative stress markers independently of age and resulted in an increase of GPx activity in both younger old and the oldest old active groups.


2019 ◽  
Vol 70 (1) ◽  
pp. 18-29 ◽  
Author(s):  
Pinar Erkekoglu ◽  
Ming-Wei Chao ◽  
Chia-Yi Tseng ◽  
Bevin P. Engelward ◽  
Ozge Kose ◽  
...  

AbstractExposure to alkyl anilines may lead to bladder cancer, which is the second most frequent cancer of the urogenital tract. 3,5-dimethylaniline is highly used in industry. Studies on its primary metabolite 3,5-dimethylaminophenol (3,5-DMAP) showed that this compound causes oxidative stress, changes antioxidant enzyme activities, and leads to death of different mammalian cells. However, there is no in vitro study to show the direct effects of 3,5-DMAP on human bladder and urothelial cells. Selenocompounds are suggested to decrease oxidative stress caused by some chemicals, and selenium supplementation was shown to reduce the risk of bladder cancer. The main aim of this study was to investigate whether selenocompounds organic selenomethionine (SM, 10 µmol/L) or inorganic sodium selenite (SS, 30 nmol/L) could reduce oxidative stress, DNA damage, and apoptosis in UROtsa cells exposed to 3,5-DMAP. 3,5-DMAP caused a dose-dependent increase in intracellular generation of reactive oxygen species, and its dose of 50 µmol/L caused lipid peroxidation, protein oxidation, and changes in antioxidant enzyme activities in different cellular fractions. The comet assay also showed single-strand DNA breaks induced by the 3,5-DMAP dose of 50 µmol/L, but no changes in double-strand DNA breaks. Apoptosis was also triggered. Both selenocompounds provided partial protection against the cellular toxicity of 3,5-DMAP. Low selenium status along with exposure to alkyl anilines can be a major factor in the development of bladder cancer. More mechanistic studies are needed to specify the role of selenium in bladder cancer.


1994 ◽  
Vol 120 (6) ◽  
pp. 374-377 ◽  
Author(s):  
K. Punnonen ◽  
M. Ahotupa ◽  
K. Asaishi ◽  
M. Hy�ty ◽  
R. Kudo ◽  
...  

2008 ◽  
Vol 28 (2) ◽  
pp. 73-81 ◽  
Author(s):  
Chandramani Pathak ◽  
Yogesh K. Jaiswal ◽  
Manjula Vinayak

Constant generation of ROS (reactive oxygen species) during normal cellular metabolism of an organism is generally balanced by a similar rate of consumption by antioxidants. Imbalance between ROS production and antioxidant defence results in an increased level of ROS, causing oxidative stress, which leads to promotion of malignancy. Queuine is a hyper-modified base analogue of guanine, found at the first anticodon position of the Q-family of tRNAs. These tRNAs are completely modified with respect to queuosine in terminally differentiated somatic cells; however, hypo-modification of Q-tRNAs is closely associated with cell proliferation. Q-tRNA modification is essential for normal development, differentiation and cellular function. Queuine is a nutrient factor for eukaryotes. It is found to promote the cellular antioxidant defence system and inhibit tumorigenesis. The activities of antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase are found to be low in the DLAT (Dalton's lymphoma ascites transplanted) mouse liver compared with normal mouse liver. However, exogenous administration of queuine to the DLAT cancerous mouse improves the activities of antioxidant enzymes. These results suggest that queuine promotes the antioxidant defence system by increasing antioxidant enzyme activities and in turn inhibits oxidative stress and tumorigenesis.


Sign in / Sign up

Export Citation Format

Share Document