Effects of exposure to 50 Hz electric field at different strengths on oxidative stress and antioxidant enzyme activities in the brain tissue of guinea pigs

2008 ◽  
Vol 84 (7) ◽  
pp. 581-590 ◽  
Author(s):  
Zerri˙n Türközer ◽  
Göknur Güler ◽  
Nesri˙n Seyhan
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 ◽  
...  

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.


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.


2009 ◽  
Vol 53 (3) ◽  
pp. 493-504 ◽  
Author(s):  
R. K. Sairam ◽  
D. Kumutha ◽  
K. Ezhilmathi ◽  
V. Chinnusamy ◽  
R. C. Meena

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