Protective effect of ascorbic acid against lipid peroxidation and oxidative damage in cardiac microsomes

1993 ◽  
Vol 126 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Mau Mukhopadhyay ◽  
Chinmay K. Mukhopadhyay ◽  
Indu B. Chatterjee
Pancreatology ◽  
2006 ◽  
Vol 6 (5) ◽  
pp. 477-485 ◽  
Author(s):  
Mukaddes Eşrefoğlu ◽  
Mehmet Gül ◽  
Burhan Ateş ◽  
Ismet Yilmaz

2007 ◽  
Vol 2 (4) ◽  
pp. 538-546
Author(s):  
Anna Gumieniczek ◽  
Hanna Hopkała ◽  
Marcin Pruchniak

AbstractIn the present study, the induction of oxidative stress was examined in the testis of alloxan-induced diabetic rabbits. In addition, the protective effect of repaglinide, an oral anti-diabetic, at a dose of 1 mg daily was studied after four and eight weeks of the treatment. For these purposes, the levels of superoxide dismutase (Cu,Zn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), glutathione (GSH), ascorbic acid (AA), lipid peroxidation products (LPO) and protein carbonyl groups (PCG) were quantified. Hyperglycemia resulted in significant increases in the antioxidative enzymes, Cu, Zn-SOD, CAT, GSH-Px, and GSSG-R after four and eight weeks, respectively. There was also an increase in GSH level, and a decrease in the level of AA. These effects were accompanied by an elevation in testicular LPO levels and PCG levels. Repaglinide was found to normalize the activity of GSSG-R and levels of GSH and AA, and blunted the increased lipid peroxidation, however no decrease in PCG levels were observed. In conclusion, some oxidative changes provoked in the testis of rabbits by hyperglycemia, were found to be reduced with repaglinide treatment at therapeutic dose.


1981 ◽  
Vol 199 (1) ◽  
pp. 259-261 ◽  
Author(s):  
John M. C. Gutteridge ◽  
Suzanne K. Paterson ◽  
Anthony W. Segal ◽  
Barry Halliwell

Lactoferrin containing physiological amounts of iron is an inhibitor of lipid peroxidation induced by iron(III) salts and ascorbic acid. It might therefore help to protect neutrophils, inflammatory foci and secretions from metal-ion-dependent oxidative damage.


2017 ◽  
Vol 42 (4) ◽  
Author(s):  
Mahgoub Mohamed Ahmed

AbstractObjective:The objective of the current study is to investigate the protective effect ofMethods:Forty adult male albino rats were divided into four groups as control,Results:The results showed that, administration of EtOH caused a significant decrease (p<0.05) in serum total protein and albumin, whereas ALT and AST and lipid peroxidation (LPO) were increased following EtOH treatment.Conclusion:had a hepatoprotective role against EtOH-induce oxidative stress and inflammation in rat liver.


Author(s):  
Sasidharan Salini ◽  
Menon Kunnathully Divya ◽  
Thomas Chubicka ◽  
Nair Meera ◽  
Devanand P. Fulzele ◽  
...  

AbstractOxidative stress in erythrocyte was induced by AAPH. The inhibition of hemolysis, membrane lipid peroxidation, and protein damage by chloroform extracts ofApproximately 95% of erythrocytes were lysed by AAPH over 3 h of incubation. Significant reduction in hemolysis was observed by the extracts, and the ICResults indicate that


1998 ◽  
Vol 17 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Syed Saleem Haider ◽  
A A Abdel-Gayoum ◽  
Mustafa El-Fakhri ◽  
Kilani M Ghwarsha

The protective effect of selenium on the neurotoxicity of vanadium in different brain regions of rats was investigated. The lipid peroxidation was significantly accentuated after intraperitoneal (i.p.) administration of vanadium (1.5 mg kg71 b.wt) for a period of 12 consecutive days to rats. The increase in lipid peroxidation was inhibited by selenium treatment (0.02 mg kg71 b.wt., i.p.) for 12 consecutive days. Vanadium exposure produced a decrease in nonprotein sulfhydryl group. Selenium treatment prevented the depression in nonprotein sulfhydryl group in all the brain regions of the vanadium exposed rats. The concentration of ascorbic acid was decreased after co-administration of selenium and vanadium. These results suggest that selenium protects neuronal cells against neurotoxic effects of vanadium by maintaining the availability of antioxidant nonprotein sulfhydryl groups. The decrease in ascorbic acid levels may have been due to its consumption in forming complexes with vanadium.


Sign in / Sign up

Export Citation Format

Share Document