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Differential effects of hyperoxia and hydrogen peroxide on DNA damage, polyadenosine diphosphate‐ribose polymerase activity, and nicotinamide adenine dinucleotide and adenosine triphosphate contents in cultured endothelial cells and fibroblasts
Author(s) -
Junod Alain F.,
Jornot Lan,
Petersen Hilke
Publication year - 1989
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041400121
Subject(s) - nad+ kinase , poly adp ribose polymerase , hyperoxia , adenosine triphosphate , oxidative stress , nicotinamide adenine dinucleotide , biochemistry , microbiology and biotechnology , nicotinamide , dna damage , nicotinamide adenine dinucleotide phosphate , chemistry , polymerase , adenosine , biology , dna , enzyme , oxidase test , oxygen , organic chemistry
The effects of oxidative stress on DNA damage and associated reactions, increased polyadenosine diphosphate‐ribose polymerase (PARP) activity and decreased nicotinamide adenine dinucleotide (NAD) and adenosine triphosphate (ATP) contents, have been tested in primary cultures of porcine aortic endothelial cells. The cells were treated with 50‐500 μM H 2 O 2 for 20 min or 100 μM paraquat for 3 days or were exposed to 95% O 2 for 2 and 5 days. The administration of 250‐500 μM H 2 O 2 resulted in a marked increase in PARP activity and a profound depletion of ATP and NAD. Although hyperoxia had no effect on PARP activity and reduced only slightly the ATP and NAD stores, it markedly reduced the ability of endothelial cells to increase PARP activity upon exposure to DNase. Paraquat had a similar effect. Human dermal fibroblasts were also exposed to 50‐500 μM H 2 O 2 for 20 min or 95% O 2 for 5 days. Their response to H 2 O 2 differed from that of endothelial cells by their ability to maintain the ATP content at a normal level. Fibroblasts were also insensitive to the effect of hyperoxia. These results suggest that the oxidant‐related DNA damage is a function of the type of oxidative stress used and may be cell‐specific.