Chronic oxidative stress as a mechanism for radiation nephropathy. Radiat Res 2009 Feb;171(2):164-72
Date
03/10/2009Pubmed ID
19267541Pubmed Central ID
PMC2664164DOI
10.1667/RR1454.1Scopus ID
2-s2.0-59649097666 (requires institutional sign-in at Scopus site) 40 CitationsAbstract
Suppression of the renin-angiotensin system has proven efficacy for mitigation and treatment of radiation nephropathy, and it has been hypothesized that this efficacy is due to suppression of radiation-induced chronic oxidative stress. It is known that radiation exposure leads to acute oxidative stress, but direct evidence for radiation-induced chronic renal oxidative stress is sparse. We looked for evidence of oxidative stress after total-body irradiation in a rat model, focusing on the period before there is physiologically significant renal damage. No statistically significant increase in urinary 8-isoprostane (a marker of lipid peroxidation) or carbonylated proteins (a marker of protein oxidation) was found over the first 42 days after irradiation, while a small but statistically significant increase in urinary 8-hydroxydeoxy-guanosine (a marker of DNA oxidation) was detected at 35-55 days. When we examined renal tissue from these animals, we found no significant increase in either DNA or protein oxidation products over the first 89 days after irradiation. Using five different standard methods for detecting oxidative stress in vivo, we found no definitive evidence for radiation-induced renal chronic oxidative stress. If chronic oxidative stress is part of the pathogenesis of radiation nephropathy, it does not leave widespread or easily detectable evidence behind.
Author List
Lenarczyk M, Cohen EP, Fish BL, Irving AA, Sharma M, Driscoll CD, Moulder JEMESH terms used to index this publication - Major topics in bold
AnimalsBlood Urea Nitrogen
Bone Marrow Transplantation
Deoxyguanosine
Dinoprost
Electrophoresis, Polyacrylamide Gel
Immunohistochemistry
Kidney Diseases
Models, Animal
Oxidative Stress
Rats
Whole-Body Irradiation
