Protective role of zinc in ameliorating the arsenic-induced oxidative stress and histological changes in rat liver

2009 ◽  
Vol 189 ◽  
pp. S206
Author(s):  
Ashok Kumar ◽  
Mohan Lal Garg ◽  
Shaoli Majumdar ◽  
Davinder Kumar Dhawan
2005 ◽  
Vol 5 (9) ◽  
pp. 1397-1405 ◽  
Author(s):  
Rita Rezzani ◽  
Barbara Buffoli ◽  
Luigi Rodella ◽  
Alessandra Stacchiotti ◽  
Rossella Bianchi

2006 ◽  
Vol 291 (1-2) ◽  
pp. 155-160 ◽  
Author(s):  
Mehmet Sahin ◽  
Hakan Cam ◽  
Seref Olgar ◽  
Sevket Ercan Tunc ◽  
Cagatay Arslan ◽  
...  

2005 ◽  
Vol 156 (2-3) ◽  
pp. 101-111 ◽  
Author(s):  
Anil K Bansal ◽  
Manju Bansal ◽  
Giridhar Soni ◽  
Deepak Bhatnagar

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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