The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat heart and ameliorating role of vitamin E and vitamin C

2006 ◽  
Vol 22 (6) ◽  
pp. 455-461 ◽  
Author(s):  
O. Akturk ◽  
H. Demirin ◽  
R. Sutcu ◽  
N. Yilmaz ◽  
H. Koylu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Vitamin E ◽  
Vitamin C ◽  
Rat Heart

scholarly journals Role of vitamin E in glutathione-induced oxidant stress: methemoglobin, lipid peroxidation, and hemolysis

1977 ◽  
Vol 18 (5) ◽  
pp. 635-644
Author(s):  
N R Brownlee ◽  
J J Huttner ◽  
R V Panganamala ◽  
D G Cornwell
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Oxidant Stress

The effects of desferrioxamine on cisplatininduced lipid peroxidation and the activities of antioxidant enzymes in rat kidneys

2004 ◽  
Vol 23 (1) ◽  
pp. 29-34 ◽  
Author(s):  
G Kadikoylu ◽  
Z Bolaman ◽  
S Demir ◽  
M Balkaya ◽  
N Akalin ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Vitamin C ◽  
Isotonic Saline ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Group V ◽  
Super Oxide Dismutase ◽  
Cervical Dislocation ◽  
Rat Kidneys

Cisplatin-induced nephrotoxicity is associated with an increase in lipid peroxidation and oxygen free radicals in rat kidneys. In this study, the effects of desferrioxamine were compared to vitamin C and E on cisplatin-induced lipid peroxidation and antioxidant enzyme activities in rat kidneys. Rats were divided into five groups, with 15 Wistar rats in each group. In the control group, rats received 1 mL/100 g isotonic saline solution intraperitoneally (i.p.). In Group II, 10 mg/kg cisplatin i.p. was injected to rats. Thirty minutes before the same dosage of cisplatin administration, 100 mg/kg i.p. vitamin C or E was given to rats in groups III and IV, respectively. Rats in Group V received 250 mg/kg desferrioxamine i.p., before the same dose of cisplatin administration. All rats were killed by cervical dislocation after 72 hours. The kidneys were immediately removed and washed in cold saline. Spectrophotometric method was used for all analyses. While catalase, glutathione reductase (GR), and super oxide dismutase (SOD) levels were found to be significantly decreased (P B < 0.001), malondialdehyde (MDA) (P < 0.05) and hydrogen peroxide (H2O2) (P < 0.001) levels were significantly increased in the cisplatin group when compared to the controls. MDA levels were decreased by desferrioxamine (P < 0.005) as well as vitamin C and E (P < 0.05 and P < 0.001, respectively). These three compounds induced a significant increase in SOD levels (P B < 0.05), but only in the vitamin C group, were SOD levels not significantly different than the levels of the controls (P > 0.05). In the desferrioxamine (P < 0.05), vitamin C and E groups (P < 0.001 for both), the cisplatin elevated H2O2 levels were decreased. None of these drugs had any effect on GR and catalase levels (P > 0.05). Desferrioxamine is useful to prevent cisplatin-induced lipid peroxidation, however, vitamin C and E are more effective on antioxidant enzymes than desferrioxamine.

Beneficial effects of vitamin C and vitamin E on reserpine-induced oral dyskinesia in rats: Critical role of striatal catalase activity

2005 ◽  
Vol 48 (7) ◽  
pp. 993-1001 ◽  
Author(s):  
Rulian Ricardo Faria ◽  
Vanessa Costhek Abílio ◽  
Christian Grassl ◽  
Cibele Cristina Chinen ◽  
Luciana Takahashi Ribeiro Negrão ◽  
...  
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Catalase Activity ◽  
Critical Role ◽  
Beneficial Effects ◽  
Oral Dyskinesia

The effects of organophosphate insecticide diazinon on malondialdehyde levels and myocardial cells in rat heart tissue and protective role of vitamin E

2006 ◽  
Vol 86 (2) ◽  
pp. 93-98 ◽  
Author(s):  
Ayse Ogutcu ◽  
Meltem Uzunhisarcikli ◽  
Suna Kalender ◽  
Dilek Durak ◽  
Fatma Bayrakdar ◽  
...  
Keyword(s):  
Vitamin E ◽  
Rat Heart ◽  
Heart Tissue ◽  
Protective Role ◽  
Myocardial Cells ◽  
Organophosphate Insecticide

scholarly journals A CRITICAL REVIEW ON HYPOTHESIS, PATHOPHYSIOLOGY OF SCHIZOPHRENIA, AND ROLE OF VITAMINS IN ITS MANAGEMENT

2018 ◽  
Vol 11 (8) ◽  
pp. 25
Author(s):  
Rosmi Jose ◽  
Venketeswaramurthy N ◽  
Sambath Kumar R
Keyword(s):  
Vitamin D ◽  
Vitamin E ◽  
Vitamin C ◽  
Critical Review ◽  
Methylenetetrahydrofolate Reductase ◽  
Vitamin Supplementation ◽  
Vitamin B ◽  
High Dose ◽  
Main Effects

This review describes about the literatures addressing the role of vitamin supplementation in schizophrenia. Evidence is suggesting that vitamin supplementation includes Vitamin A, Vitamin D, Vitamin E, Vitamin B complex, and Vitamin C may be important in treatment. In schizophrenia, patients may have increased level of homocysteine (Hcy), due to the polymorphism in methylenetetrahydrofolate reductase and hypofunction of N-methyl-D-aspartate receptors. The vitamins main effects are reduced the Hcy level and maintain dopamine and serotonin levels. Add-on treatment with high-dose B vitamins including B6, B9, and B12 and also Vitamin D can significantly reduce symptoms of schizophrenia more than standard treatments alone.

Role of Vitamin E and Lipid Peroxidation in Atherosclerosis

Vitamin E ◽  
2015 ◽  
pp. 243-247
Author(s):  
Sampath Parthasarathy
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E

Protective role of melatonin and a combination of vitamin C and vitamin E on lung toxicity induced by chlorpyrifos-ethyl in rats

2002 ◽  
Vol 54 (2) ◽  
pp. 97-108 ◽  
Author(s):  
Erdal Karaoz ◽  
Fatih Gultekin ◽  
Mehmet Akdogan ◽  
Meral Oncu ◽  
Alpaslan Gokcimen
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Protective Role ◽  
Lung Toxicity ◽  
Chlorpyrifos Ethyl

scholarly journals Sex Differences in Postischemic Neuronal Necrosis in Gerbils

1991 ◽  
Vol 11 (2) ◽  
pp. 292-298 ◽  
Author(s):  
Edward D. Hall ◽  
Kay E. Pazara ◽  
Kelley L. Linseman
Keyword(s):  
Lipid Peroxidation ◽  
Cerebral Cortex ◽  
Vitamin E ◽  
Protective Efficacy ◽  
Neuronal Population ◽  
Mongolian Gerbils ◽  
Neuronal Necrosis ◽  
Male And Female ◽  
Endogenous Estrogen

Twenty-four hour postischemic neuronal necrosis was compared in male vs. female Mongolian gerbils subjected to a 3-h period of severe incomplete hemispheric ischemia produced by unilateral carotid occlusion. The incidence of stroke-prone males was 42.9% versus 26.7% for the females. Among the stroke-prone animals, the males displayed significantly greater neuronal necrosis at 24 h after ischemia compared to the females in the cerebral cortex and CA, region of the hippocampus. In the CA, region of the stroke-prone males, only 2.0% of the normal neuronal population remained by 24 h compared to 36.8% in the stroke-prone females (p < 0.02). In the cerebral cortex, the males had only 19.9% of normal versus 58.2% in the females (p < 0.05). In a second series of mechanistic experiments, no differences in cortical blood flow (CBF) were disclosed between preselected male and female stroke-prone animals before, during, or for 2 h after ischemia. As with the CBF, the extent of cortical extracellular hypocalcia during ischemia did not differ significantly. However, the degree of postischemic recovery of cortical extracellular calcium was significantly better in the females from 30 min to 2 h after reperfusion. In the same experiments, hemispheric vitamin E levels were measured at the 2 h time point as an index of postischemic brain lipid peroxidation. No difference in baseline vitamin E levels was observed between male and female sham-operated gerbils. In the males subjected to 3 h of ischemia plus 2 h of reperfusion, the hemispheric vitamin E decreased by 43.5% compared to the sham-operated males. In contrast, the females displayed only a 4.2% decline (p < 0.05 versus males). Previous studies showing the protective efficacy of antioxidants in this model have suggested an important role of oxygen radical-induced lipid peroxidation. Thus, it is proposed that the lesser ischemic vulnerability of females may be based upon an antioxidant effect of endogenous estrogen. Indeed, estrogen was found to be a more potent inhibitor of iron-catalyzed lipid peroxidation in brain tissue than vitamin E.

Sign in / Sign up

Export Citation Format

Share Document