Modification by vitamin E and exercise of oxidative stress in regions of aging rat brain: Studies on superoxide dismutase isoenzymes and protein oxidation status

2006 ◽  
Vol 41 (8) ◽  
pp. 753-763 ◽  
Author(s):  
A.B. Jolitha ◽  
M.V.V. Subramanyam ◽  
S. Asha Devi
Author(s):  
Pradeesh S ◽  
Swapna T S

Objective: The main aim of this study was to evaluate the antioxidants present in Sesbania grandiflora (L.) Pers. belongs to the family Fabaceae.Methods: Fresh samples were used for the analysis of antioxidants such as total phenol, carotenoids, Vitamin-A, Vitamin-C, Vitamin-E, peroxidase (POD), catalase (CAT), superoxide dismutase (SOD), ascorbate peroxidase, monodehydroascorbate reductase, and glutathione reductase by standard estimation methods.Results: Present studies revealed that this wild leafy plant has numerous antioxidant factors that destroying the free radicals that damage the cells.Conclusion: S. grandiflora contain many enzymatic and non-enzymatic antioxidants and could be a good source of dietary antioxidants which play an important role in the prevention of diseases associated with oxidative stress.


1998 ◽  
Vol 76 (10-11) ◽  
pp. 952-960 ◽  
Author(s):  
Peter M Tiidus ◽  
Eric Bombardier ◽  
Nick Hidiroglou ◽  
Rene Madere

Estrogen can putatively act as an antioxidant and protect tissues from exercise-induced oxidative stress. To test the in vivo efficacy of estrogen, the effects of 2 weeks of daily estrogen (40 µg·kg-1 body weight beta-estradiol 3-benzoate) injection on indices of immediate postexercise oxidative stress and antioxidant status were determined in adult male rats, with and without 8 weeks of prior dietary vitamin E deprivation. The treadmill running protocol (60 min at 21 m·min-1, 12% grade) induced significant oxidative stress as indicated by muscle glutathione status. Estrogen administration had little effect on postexercise tissue glutathione status, superoxide dismutase and glutathione peroxidase activity, and vitamin E levels. Estrogen administration induced significant reductions in muscle, liver, and heart vitamin C concentrations following exercise, as well as in unexercised male rats. Tissue vitamin C loss was not directly mediated through liver glycogen or glutathione status. Thus, estrogen administration generally did not appear to influence postexercise tissue indices of oxidative stress or antioxidant status and may have contributed to a decline in overall antioxidant protection by inducing losses in tissue vitamin C content.Key words: glutathione, vitamin E, muscle, superoxide dismutase, glutathione peroxidase.


2008 ◽  
Vol 41 (6) ◽  
pp. 423-430 ◽  
Author(s):  
A S R Araujo ◽  
P Schenkel ◽  
A T Enzveiler ◽  
T R G Fernandes ◽  
W A Partata ◽  
...  

This study was conducted to test whether oxidative stress activates the intracellular protein kinase B (AKT1) signaling pathway, which culminates with cardiac hypertrophy in experimental hyperthyroidism. Male Wistar rats were divided into four groups: control, vitamin E, thyroxine (T4), and T4+vitamin E. Hyperthyroidism was induced by T4 administration (12 mg/l in drinking water for 28 days). Vitamin E treatment was given during the same period via s.c. injections (20 mg/kg per day). Morphometric and hemodynamic parameters were evaluated at the end of the 4-week treatment period. Protein oxidation, redox state (reduced glutathione, GSH/glutathione dissulfide, GSSG), vitamin C, total radical-trapping antioxidant potential (TRAP), hydrogen peroxide (H2O2), and nitric oxide metabolites (NOX) were measured in heart homogenates. The p-AKT1/AKT1 ratio, p-glycogen-synthase kinase (GSK)3B/GSK3B ratio, FOS, and JUN myocardial protein expression were also quantified by western blot after 4 weeks. Increases in biochemical parameters, such as protein oxidation (41%), H2O2 (62%), and NOX (218%), and increase in the left ventricular end-diastolic pressure were observed in the T4 group. T4 treatment also caused a decrease in GSH/GSSG ratio (83%), vitamin C (34%), and TRAP (55%). These alterations were attenuated by vitamin E administration to the hyperthyroid rats. Expression of p-AKT1/AKT1, p-GSK3B/GSK3B, FOS, and JUN were elevated in the T4 group (by 69, 37, 130, and 33% respectively), whereas vitamin E administration promoted a significant reduction in their expression. These results indicate that oxidative stress plays an important role in cardiac hypertrophy, and suggest redox activation of AKT1 and JUN/FOS signaling pathways with H2O2 acting as a possible intracellular mediator in this adaptive response to experimental hyperthyroidism.


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