Phospholipid spectrum and lipid peroxidation in cell membranes of brain tissue in thymectomized rats

1994 ◽  
Vol 118 (1) ◽  
pp. 701-703
Author(s):  
V. Yu. Serebrov ◽  
O. A. Timin
Keyword(s):  
Lipid Peroxidation ◽  
Brain Tissue ◽  
Cell Membranes

Lipid Peroxidation and Nitrite plus Nitrate Levels in Brain Tissue from Patients with Alzheimer’s Disease

Gerontology ◽  
2000 ◽  
Vol 46 (4) ◽  
pp. 179-184 ◽  
Author(s):  
Maira DiCiero Miranda ◽  
Veralice M.S. de Bruin ◽  
Marcus R. Vale ◽  
Glauce S.B. Viana
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lipid Peroxidation ◽  
Brain Tissue

scholarly journals Decreased glucorticoid sensitivity as a factor of stressogenic shifts in the activity of monoamine oxidase, lipid peroxidation, and behavior in rats

2003 ◽  
Vol 49 (5) ◽  
pp. 48-51 ◽  
Author(s):  
I. A. Volchegorsky ◽  
V. E. Tseilikman ◽  
D. S. Smirnov ◽  
S. A. Ship ◽  
A. V. Borisenkov
Keyword(s):  
Lipid Peroxidation ◽  
Monoamine Oxidase ◽  
Brain Tissue ◽  
Behavioral Disorders ◽  
Immobilization Stress ◽  
Glucocorticoid Hormones ◽  
And Behavior ◽  
The Brain

Four episodes of immobilization stress cause a decrease in the sensitivity to glucocorticoid hormones, followed by anxiogenic be­havioral disorders, enhanced monoamine oxidase-В (МАО-В) activity and simultaneously increased lipid peroxidation (LPO) in the brain tissue of rats. Concurrently, there is an increase in renal МАО-В activity, as well as renal and hepatic accumulation of LPO products. Administration of kenalog (2 mg/kg), a phar­macological analogue of glucocorticoid hormones, prevents the poststress МАО-В activation and LPO and attenuates anxiogen­ic behavioral disorders in the rats.

Lipid peroxidation in brain tissue in vitro: Antioxidant effects of barbiturates

1979 ◽  
Vol 105 (4) ◽  
pp. 527-529 ◽  
Author(s):  
DAVID S. SMITH ◽  
STIG REHNCRONA ◽  
EVA WESTERBERG ◽  
BJORN AKESSON ◽  
BO K. SIESJÖ
Keyword(s):  
Lipid Peroxidation ◽  
Brain Tissue ◽  
Antioxidant Effects

Lycopene modulates cholinergic dysfunction, Bcl-2/Bax balance, and antioxidant enzymes gene transcripts in monosodium glutamate (E621) induced neurotoxicity in a rat model

2016 ◽  
Vol 94 (4) ◽  
pp. 394-401 ◽  
Author(s):  
Kadry Sadek ◽  
Tarek Abouzed ◽  
Sherif Nasr
Keyword(s):  
Lipid Peroxidation ◽  
Brain Tissue ◽  
Creatine Phosphokinase ◽  
Monosodium Glutamate ◽  
Serum Cholinesterase ◽  
Glutathione S Transferase ◽  
Group Iii ◽  
Group I ◽  
Male Wistar Rats ◽  
Induced Apoptosis

The effect of monosodium glutamate (MSG) on brain tissue and the relative ability of lycopene to avert these neurotoxic effects were investigated. Thirty-two male Wistar rats were distributed into 4 groups: group I, untreated (placebo); group II, injected with MSG (5 mg·kg−1) s.c.; group III, gastrogavaged with lycopene (10 mg·kg−1) p.o.; and group IV received MSG with lycopene with the same mentioned doses for 30 days. The results showed that MSG induced elevation in lipid peroxidation marker and perturbation in the antioxidant homeostasis and increased the levels of brain and serum cholinesterase (ChE), total creatine phosphokinase (CPK), creatine phosphokinase isoenzymes BB (CPK-BB), and lactate dehydrogenase (LDH). Glutathione S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) activities and gene expression were increased and glutathione content was reduced in the MSG-challenged rats, and these effects were ameliorated by lycopene. Furthermore, MSG induced apoptosis in brain tissues reflected in upregulation of pro-apoptotic Bax while lycopene upregulated the anti-apoptotic Bcl-2. Our results indicate that lycopene appears to be highly effective in relieving the toxic effects of MSG by inhibiting lipid peroxidation and inducing modifications in the activity of cholinesterase and antioxidant pathways. Interestingly, lycopene protects brain tissue by inhibiting apoptosis signaling induced by MSG.

Lipid peroxidation in brain tissue in vitro: Effects on phospholipids and fatty acids

1979 ◽  
Vol 105 (4) ◽  
pp. 524-526 ◽  
Author(s):  
EVA WESTERBERG ◽  
BJÖRN ÅKESSON ◽  
STIG REHNCRONA ◽  
DAVID S. SMITH ◽  
BO K. SIESJÖ
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Brain Tissue ◽  
In Vitro Effects

Lability of red blood cell membranes to lipid peroxidation: Application to humans fed polyunsaturated lipids

Lipids ◽  
1990 ◽  
Vol 25 (2) ◽  
pp. 111-114 ◽  
Author(s):  
Cesar G. Fraga ◽  
A. L. Tappel ◽  
Brian E. Leibovitz ◽  
Franz Kuypers ◽  
Daniel Chiu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Cell Membranes ◽  
Red Blood Cell Membranes ◽  
Polyunsaturated Lipids

Lipid peroxidation blockade: neuroprotection from cell membranes to humans

1998 ◽  
Vol 15 (Supplement 17) ◽  
pp. 16-17
Author(s):  
J. S. Althaus ◽  
E. D. Hall ◽  
P. F. VonVoigtlander
Keyword(s):  
Lipid Peroxidation ◽  
Cell Membranes

scholarly journals Trigonella foenum-graecum seeds extract plays a beneficial role on brain antioxidant and oxidative status in alloxan-induced Wistar rats

2020 ◽  
Vol 4 (2) ◽  
pp. 83-89
Author(s):  
Jangampalli Adi Pradeepkiran ◽  
Venkata Subbaiah Nandyala ◽  
Matcha Bhaskar
Keyword(s):  
Lipid Peroxidation ◽  
Brain Tissue ◽  
Dehydrogenase Activity ◽  
Tap Water ◽  
Antioxidant Properties ◽  
Diabetic Rats ◽  
Male Rats ◽  
Control Group ◽  
Lactate Dehydrogenase Activity ◽  
Trigonella Foenum Graecum

Abstract Context Trigonella foenum-graecum (TriFG) exhibits increased scavenger enzymatic activities and reduces the production of reactive oxygen species in diabetic rats. Objective The present study was aimed to investigate the effect of TriFG on lipid peroxidation levels and antioxidant status in brain tissue of rats exposed to alloxan. Materials and Methods Healthy male rats (180 ± 10 g) were allocated into five groups. Animals in group 1 maintained on normal tap water served as controls and rats in groups 2, 3, 4, and 5 were treated as experimental groups. Rats in group 2 were intraperitoneally injected with alloxan (120 mg/kg BW) and treated as diabetic rats, whereas rats in groups 3 and 4 were maintained on same experimental regimen as that of rats in groups 1 and 2, respectively, and in addition, they were orally gavaged with herbal extracts of TriFG (0.25 g/kg BW). Diabetic rats treated with glibenclamide in group 5 were used as positive controls. Results and Discussion Significant (P < 0.001) increase in the antioxidant enzymes with a significant (P < 0.001) decrease in the lipid peroxidation levels were observed in the brain tissue of diabetic rats treated with TriFG extract as compared to diabetic and glibenclamide-treated rats. No significant changes were observed in pro- and antioxidant levels in brain tissue of rats treated with TriFG extract alone when compared to normal rats. In diabetic rats, brain mitochondrial and cytosolic enzymes like succinate dehydrogenase, glutamate dehydrogenase, and glucose-6-phosphate dehydrogenase activity levels were significantly (P < 0.05) decreased with reversely increased was observed in lactate dehydrogenase activity (P < 0.05). Conclusions The findings of the present study suggested that TriFG, through its antioxidant properties, protects brain tissue by mitigating oxidative stress induced by alloxan-exposed rats. TriFG extract significantly increased the antioxidant and oxidative properties in diabetic rats when compared with the control group rats.

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