Mechanisms of Oxidant Injury of Cells

2015 ◽  
pp. 150-160
Author(s):  
I. U. Schraufst�tter ◽  
P. A. Hyslop ◽  
J. Jackson ◽  
Charles C. Cochrane
Keyword(s):  
Oxidant Injury

scholarly journals Role of intrinsic antioxidant enzymes in renal oxidant injury

1990 ◽  
Vol 38 (2) ◽  
pp. 282-288 ◽  
Author(s):  
Toshimasa Yoshioka ◽  
Teresa Bills ◽  
Tracy Moore-Jarrett ◽  
Harry L. Greene ◽  
Ian M. Burr ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Oxidant Injury

scholarly journals Effect of pyruvate on oxidant injury to isolated and cellular DNA

1994 ◽  
Vol 45 (1) ◽  
pp. 166-176 ◽  
Author(s):  
Karl A. Nath ◽  
Helen Enright ◽  
Louise Nutter ◽  
Michael Fischereder ◽  
Jing-nan Zou ◽  
...  
Keyword(s):  
Oxidant Injury ◽  
Cellular Dna

Dang-Gui Buxue Tang Protects against Oxidant Injury by Enhancing Cellular Glutathione in H9c2 Cells: Role of Glutathione Synthesis and Regeneration

Planta Medica ◽  
2007 ◽  
Vol 73 (2) ◽  
pp. 134-141 ◽  
Author(s):  
Po Chiu ◽  
Hoi Leung ◽  
Ada Siu ◽  
Michel Poon ◽  
Tina Dong ◽  
...  
Keyword(s):  
H9c2 Cells ◽  
Oxidant Injury ◽  
Glutathione Synthesis

Expression of human Mn SOD in Chinese hamster ovary cells confers protection from oxidant injury

1993 ◽  
Vol 264 (6) ◽  
pp. L598-L605
Author(s):  
B. Warner ◽  
R. Papes ◽  
M. Heile ◽  
D. Spitz ◽  
J. Wispe
Keyword(s):  
Chinese Hamster Ovary ◽  
Cho Cells ◽  
Chinese Hamster Ovary Cells ◽  
Lethal Dose ◽  
Chinese Hamster ◽  
Eukaryotic Expression ◽  
Wild Type ◽  
Oxidant Injury ◽  
Sod Activity ◽  
Recombinant Cho Cells

Manganese superoxide dismutase (Mn SOD) is an important component of antioxidant defense in aerobic cells because of its location in the mitochondria, a significant source of oxygen radicals and an important target of oxidant injury. To test the hypothesis that increased mitochondrial Mn SOD protects from oxidant injury, Chinese hamster ovary (CHO) cells were transfected with a eukaryotic expression vector containing the human Mn SOD cDNA. In recombinant CHO cells, Mn SOD activity was increased threefold over wild-type controls. Acute survival during paraquat exposure (0–500 microM) was significantly improved in CHO cells expressing human Mn SOD, with 71% of recombinant CHO cells surviving at the 50% lethal dose (LD50) for wild-type CHO controls. Cell growth following exposure to paraquat (100 microM) was also significantly improved in recombinant CHO cells. CHO cells expressing human Mn SOD continued to grow and divide after paraquat exposure, whereas growth of wild-type CHO cells was negligible. Protection against oxidant-induced injury was directly related to increased Mn SOD, occurring in the absence of changes in other antioxidant enzymes including catalase, Cu,Zn SOD, and glutathione associated cellular antioxidant mechanisms. We conclude that increased expression of human Mn SOD in vitro directly confers protection against oxidant injury.

scholarly journals Fight-or-flight: murine unilateral ureteral obstruction causes extensive proximal tubular degeneration, collecting duct dilatation, and minimal fibrosis

2012 ◽  
Vol 303 (1) ◽  
pp. F120-F129 ◽  
Author(s):  
Michael S. Forbes ◽  
Barbara A. Thornhill ◽  
Jordan J. Minor ◽  
Katherine A. Gordon ◽  
Carolina I. Galarreta ◽  
...  
Keyword(s):  
Renal Disease ◽  
Ureteral Obstruction ◽  
Volume Fraction ◽  
Interstitial Fibrosis ◽  
Unilateral Ureteral Obstruction ◽  
Oxidant Injury ◽  
Superoxide Formation ◽  
Atubular Glomeruli ◽  
Proximal Tubular ◽  
Fight Or Flight

Unilateral ureteral obstruction (UUO) is the most widely used animal model of progressive renal disease. Although renal interstitial fibrosis is commonly used as an end point, recent studies reveal that obstructive injury to the glomerulotubular junction leads to the formation of atubular glomeruli. To quantitate the effects of UUO on the remainder of the nephron, renal tubular and interstitial responses were characterized in mice 7 and 14 days after UUO or sham operation under anesthesia. Fractional proximal tubular mass, cell proliferation, and cell death were measured by morphometry. Superoxide formation was identified by nitro blue tetrazolium, and oxidant injury was localized by 4-hydroxynonenol and 8-hydroxydeoxyguanosine. Fractional areas of renal vasculature, interstitial collagen, α-smooth muscle actin, and fibronectin were also measured. After 14 days of UUO, the obstructed kidney loses 19% of parenchymal mass, with a 65% reduction in proximal tubular mass. Superoxide formation is localized to proximal tubules, which undergo oxidant injury, apoptosis, necrosis, and autophagy, with widespread mitochondrial loss, resulting in tubular collapse. In contrast, mitosis and apoptosis increase in dilated collecting ducts, which remain patent through epithelial cell remodeling. Relative vascular volume fraction does not change, and interstitial matrix components do not exceed 15% of total volume fraction of the obstructed kidney. These unique proximal and distal nephron cellular responses reflect differential “fight-or-flight” responses to obstructive injury and provide earlier indexes of renal injury than do interstitial compartment responses. Therapies to prevent or retard progression of renal disease should include targeting proximal tubule injury as well as interstitial fibrosis.

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