Effects of omega-3 PUFA on the vitamin E and glutathione antioxidant defense system in individuals at ultra-high risk of psychosis

2015 ◽  
Vol 101 ◽  
pp. 15-21 ◽  
Author(s):  
Stefan Smesny ◽  
Berko Milleit ◽  
Miriam R. Schaefer ◽  
Uta-Christina Hipler ◽  
Christine Milleit ◽  
...  
Keyword(s):  
Vitamin E ◽  
High Risk ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Omega 3 ◽  
Defense System ◽  
Ultra High Risk

scholarly journals Effects of Omega - 3 Fatty Acids on Kidney Antioxidant Defense System: An Experimental Study

2012 ◽  
Vol 1 (2) ◽  
pp. 70-74
Author(s):  
Burak Gulcen ◽  
Omur Karaca ◽  
Murat Abdulgani Kus ◽  
Dilara Kaman ◽  
Murat Ogeturk ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Experimental Study ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Defense System

Endotoxin treatment protects vitamin E-deficient rats from pulmonary O2 toxicity

1984 ◽  
Vol 247 (3) ◽  
pp. R520-R526
Author(s):  
L. Frank ◽  
K. Neriishi
Keyword(s):  
Vitamin E ◽  
Antioxidant Defense ◽  
Protective Action ◽  
Antioxidant Defense System ◽  
Antioxidant Vitamin ◽  
Defense System ◽  
Lethal Time ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Increased Susceptibility ◽  
Stimulation Of

Endotoxin treatment in normal rats has a marked protective effect against O2 toxicity (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47: 577-581, 1979 and 51: 577-583, 1981), and endotoxin's protective action is associated with stimulation of the lung's enzymatic antioxidant defense system (superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase). Vitamin E-deficient animals are especially sensitive to hyperoxidant stresses, including pulmonary O2 toxicity. In these studies we tested whether endotoxin could reverse the increased susceptibility of vitamin E-deficient rats to hyperoxic challenge. We found that untreated vitamin E-deficient rats do succumb more readily to O2 toxicity [0/11 alive at 72 h in greater than 95% O2, lethal time for 50% of the animals (LT50) = 50 h] than rats fed a regular diet (4/14 alive, LT50 = 69 h). In contrast, 15 of 16 vitamin E-deficient rats treated with endotoxin survived the same O2 exposures (P less than 0.001) and showed significantly reduced pulmonary edema compared with the other groups. The endotoxin-treated vitamin E-deficient group was also the only one to demonstrate significant elevations of all the antioxidant enzymes during O2 exposure, suggesting that the antioxidant enzyme defenses of the lung have a more primary and important role in prevention of O2-induced lung injury than the lipid-associated antioxidant, vitamin E.

Cadmium-induced lipid peroxidation and changes in antioxidant defense system in the rat testes: Protective role of coenzyme Q10 and Vitamin E

2010 ◽  
Vol 29 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Branka I. Ognjanović ◽  
Snežana D. Marković ◽  
Nataša Z. Ðorđević ◽  
Ivana S. Trbojević ◽  
Andraš Š. Štajn ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Coenzyme Q10 ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Protective Role ◽  
Defense System

scholarly journals Antioxidant Effect of the Complex Action of Vitamin E and Ethylthiosulfаnylate in the Liver and Kidneys of Rats under Conditions of Chrome(VI)-Induced Oxidative Stress

2021 ◽  
Vol 12 (2) ◽  
pp. 1405-1420
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Antioxidant Defense ◽  
Antioxidant Properties ◽  
Antioxidant Defense System ◽  
Physiological Solution ◽  
Rat Tissues ◽  
Defense System ◽  
Complex Action ◽  
Complex Effect

The aim of our study was to investigate the efficacy and benefits of the complex effect of vitamin E and ethylthiosulfanylate (ETS) on the state of the pro/antioxidant system in the liver and kidneys of rats under the condition of Cr(VI)-induced oxidative stress. Rats were divided into 8 groups. Groups received: I (control) - physiological solution (150 μl) for 7 days; II – oil solution (1 ml) for 14 days; III, IV, VII, VIII - K2Cr2O7 (2.5 mg Cr(VI)/kg body weight (b.w)) for 7 (III, IV) and for 14 (VII, VIII); V - vitamin E (20 mg/kg b.w) for 14 days; VI, VII, VIII - vitamin E in complex with ETS (100 mg/kg b.w) for 14 days. Results report that K2Cr2O7 caused Cr(VI)-induced oxidative stress due to activation of lipid peroxidation (LP) processes. Cr(VI) action for 7 days caused compensatory activation of the antioxidant defense system (AOS) in both tissues. However, the longer action of Cr(VI) was accompanied by depletion of AOS enzyme activity and GSH content. The complex effect of vitamin E and ETS reduced the intensity of Cr(VI)-induced oxidative stress in both rat tissues. Our results indicate about positive antioxidant properties of vitamin E and ETS under the condition of Cr(VI) toxicity.

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