Copyright
©The Author(s) 2015.
World J Nephrol. May 6, 2015; 4(2): 213-222
Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.213
Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.213
Figure 1 Oxidative stress and antioxidative/redox systems in red blood cells.
A part of oxygenized hemoglobin (Hb-O2) is autoxidized to methemoglobin (MetHb) and releases superoxide (O2-.), which may cause oxidative damage to RBCs. MetHb can be reduced back to Hb by methemoglobin reductase in NADPH-dependent manner. G6PD, a rate-determining enzyme in the pentose phosphate pathway, is involved in the production of NADPH that supports antioxid/redox systems as well as methemoglobin reduction by donating redox potential. G6PD deficiency affects entire antioxidative/redox systems, which can consequently accelerate the destruction of RBCs and lead to anemia. RBCs: Red blood cells. NADPH: Triphosphopyridine nucleotide.
- Citation: Fujii J, Kurahashi T, Konno T, Homma T, Iuchi Y. Oxidative stress as a potential causal factor for autoimmune hemolytic anemia and systemic lupus erythematosus. World J Nephrol 2015; 4(2): 213-222
- URL: https://www.wjgnet.com/2220-6124/full/v4/i2/213.htm
- DOI: https://dx.doi.org/10.5527/wjn.v4.i2.213