scholarly journals Protective role of l-ascorbic acid on erythrocytes subjected to oxidative stress during human aging

2009 ◽  
Vol 25 ◽  
pp. S2 ◽  
Author(s):  
A. Arora ◽  
P.K. Maurya ◽  
A. Sharma
2016 ◽  
Vol 6 (1) ◽  
pp. 39 ◽  
Author(s):  
Muneer Ahmad Dar ◽  
Rajinder Raina ◽  
Arshad Hussain Mir ◽  
Pawan Kumar Verma ◽  
Nrip Kishore Pankaj ◽  
...  

2011 ◽  
Vol 38 (3) ◽  
pp. 635-643 ◽  
Author(s):  
Ferbal Özkan ◽  
Suna Gül Gündüz ◽  
Mehmet Berköz ◽  
Arzu Özlüer Hunt ◽  
Serap Yalın

2016 ◽  
Vol 6 (2) ◽  
pp. 0-0 ◽  
Author(s):  
D. Kumar ◽  
B. Sharma ◽  
SI Rizvi

Purpose: Carbofuran toxicity on rats was studied during sub-acute exposure. This work was undertaken to evaluate the protective effect of aqueous black tea extract and vitamin C against a rat model of oxidative stress induced by treatment with carbofuran, an organocarbamate insecticide. Materials and methods: The levels of lipid peroxidation, reduced glutathione and ascorbic acid were assessed by determining the extent of oxidative stress in the erythrocytes of rats. Results: The results clearly demonstrated that the treatment of rats with sub-acute concentration of carbofuran caused significant elevation in the levels of oxidative stress and decrease in the contents of glutathione and ascorbic acid. The introduction of black tea extract and vitamin C augmented the antioxidant defense mechanism in alleviating the carbofuran induced oxidative stress. Conclusion: The findings that the pretreatment with black tea and vitamin C can mitigate carbofuran induced toxicity lend evidence that supplementation with either black tea extract and/or vitamin C have a therapeutic potential in amelioration of oxidative stress in mammalian systems


2010 ◽  
Vol 92 (5) ◽  
pp. 947-953 ◽  
Author(s):  
Rajinder Raina ◽  
Pawan K. Verma ◽  
Nrip K. Pankaj ◽  
Vinay Kant ◽  
Shahid Prawez

2021 ◽  
Vol 22 (15) ◽  
pp. 7765
Author(s):  
Youichirou Higashi ◽  
Takaaki Aratake ◽  
Takahiro Shimizu ◽  
Shogo Shimizu ◽  
Motoaki Saito

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.


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