Role of reactive oxygen species generated by NADPH oxidase in the mechanism of activation of K+-Cl--cotransport byN-ethylmaleimide in HepG2 human hepatoma cells

2001 ◽  
Vol 35 (1) ◽  
pp. 43-53 ◽  
Author(s):  
Jung-Ae Kim ◽  
Yong Soo Lee
2015 ◽  
Vol 29 (3) ◽  
pp. 479-488 ◽  
Author(s):  
Samuel Liebel ◽  
Ciro Alberto de Oliveira Ribeiro ◽  
Valéria Freitas de Magalhães ◽  
Rodrigo de Cássio da Silva ◽  
Stéfani Cibele Rossi ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Sunil Joshi ◽  
Ammon B. Peck ◽  
Saeed R. Khan

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.


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