Pathological investigation of oxidative stress in the post-genomic era
Version of Record online: 1 JUL 2007
Volume 57, Issue 8, pages 461–473, August 2007
How to Cite
Toyokuni, S. and Akatsuka, S. (2007), Pathological investigation of oxidative stress in the post-genomic era. Pathology International, 57: 461–473. doi: 10.1111/j.1440-1827.2007.02127.x
- Issue online: 1 JUL 2007
- Version of Record online: 1 JUL 2007
- Received 2 February 2007. Accepted for publication 21 March 2007.
- chromosome territory;
- reactive species
Aerobes, including humans, are consistently exposed to oxidative stress by consuming oxygen. The biological significance of oxidative stress via reactive oxygen and nitrogen species consists of two stages: reversible redox regulation and irreversible oxidative molecular damage, which are sometimes intermingled. During the past decade, many signaling cascades associated with oxidative stress have been discovered. An interaction between Keap1 and the Nrf2 transcription factor is among the most fundamental mechanisms of the defense system against oxidative or similar stress. Furthermore, it became apparent that reactive oxygen species are actively produced through enzymes such as xanthine oxidoreductase and nicotinamide adenine dinucleotide phosphate, reduced (NADPH) oxidases in non-phagocytic cells as well. The role of α-tocopherol solely as an anti-oxidant was also questioned. Now there is a long list of pathological states implicating oxidative stress. At the same time, genome projects on various species have been completed. These efforts convincingly led to a new era of oxidative stress investigation, contributing powerful strategies to select candidate genes or biomolecules. Herein are reviewed recent advances and novel concepts in this field, including oxygenomics. These fruitful results may lead to more accurate and useful pathological diagnosis and more efficient prophylaxis and therapeutic interventions on human diseases.