Nephrol Dial Transplant (2000) 15: 1127-1132
© 2000 European Renal Association-European Dialysis and Transplant Association
Invited Comment
Role of reactive oxygen species in glomerulonephritis
1 Department of Nephrology, Medical School, Hannover, and 2 Department of Cellular and Molecular Pathology, German Cancer Research Center (DKFZ) Heidelberg, Germany
Introduction to reactive oxygen species and their pathophysiology
Small amounts of reactive oxygen species (ROS) are constantly produced in aerobic metabolism and have important roles in normal cell physiology e.g. signal transduction pathways. However, in pathophysiological conditions with increased levels of ROS, these molecules become relevant factors in the initiation and amplification of deleterious processes observed in inflammation, oncogenesis, and degenerative diseases [1,2].
ROS are products of the partial reduction of oxygen and can be generated by enzymatic and non-enzymatic reactions within cells and at the cell membrane [3,4]. Enzymes that generate ROS are termed oxidative enzymes (Table 1
) [5–16]. Major ROS are depicted in Figure 1, which also shows the important reactions and catalysts involved. Hypochlorous acid produced by myeloperoxidase and hydroxyl radical (OH·), which evolves from non-enzymatic reactions dependent on the availability of the free metal ions Fe2+ or Cu+,
ROS in glomerular disease
Equivalents to minimal-change glomerulopathy (MCG)
Equivalent to mesangioproliferative GN
Equivalent to membranous GN
Equivalent to focal segmental necrotizing GN
Lessons from the animal studies and applications to human glomerular disease
Therapeutic modulation of oxidative injury in human GN
Inhibition of increased ROS generation
Enhanced degradation of ROS
Acknowledgments
Notes
References
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