Humic acid-mediated oxidative damages to human erythrocytes: a possible mechanism leading to anemia in Blackfoot disease.
Humic acid (HA) has been proposed as a factor that causes Blackfoot disease, an endemic peripheral vascular disease prevailing in the southwest coast of Taiwan. However, the relationship between HA and anemia associated with Blackfoot disease remains unclear. In this study, we showed that HA imposed damages on human red blood cells (RBCs), which were manifested as reduction in deformability of RBCs and hemolysis. At concentrations ranging from 10 to 100 microg/ml, HA caused lipid peroxidation in a dose-dependent manner. Such changes were accompanied by a depletion of glutathione and a reduction in activities of the antioxidant enzymes including catalase, superoxide dismutase, and glucose-6-phosphate dehydrogenase. These results indicate that HA initiates oxidative stress on RBCs and results in their dysfunction. Consistent with our previous findings, the present study supports the notion that HA plays an important role in the pathogenesis of Blackfoot disease.
Cheng
M L
ML
Department of Biochemistry and Internal Medicine, College of Medicine, National Taiwan University, Taipei, Republic of China.
Ho
H Y
HY
Chiu
D T
DT
Lu
F J
FJ
D000740:Anemia / Q000139:chemically induced*; D004907:Erythrocyte Deformability / Q000187:drug effects; D004912:Erythrocytes / Q000187:drug effects*; D005978:Glutathione / Q000097:blood; D006461:Hemolysis; D006801:Humans; D006812:Humic Substances / Q000633:toxicity*; D015227:Lipid Peroxidation / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D016491:Peripheral Vascular Diseases / Q000139:chemically induced*; D013624:Taiwan
D006812:Humic Substances; D005978:Glutathione