TY - JOUR
T1 - Enhanced oxygen releasing capacity and oxidative stress in diabetes mellitus and diabetes mellitus-associated cardiovascular disease
T2 - A comparative study
AU - Saha, Arindam
AU - Adak, Sangeeta
AU - Chowdhury, Subhankar
AU - Bhattacharyya, Maitree
PY - 2005/11
Y1 - 2005/11
N2 - Background: Macrovascular disease, especially cardiovascular accounts for most of the mortality in patients with type 2 diabetes mellitus. We compared oxidative stress, thermal stability and oxygen releasing capacity of hemoglobin in patients with type 2 diabetes mellitus and diabetes-associated cardiovascular disease. Methods: The study was performed on 38 control subjects, 31 diabetics, 36 diabetics with cardiovascular complications, and 33 non-diabetic cardiovascular subjects. Results: Enhanced oxidative stress was shown by an increased protein carbonyl content observed both in plasma and in hemolysate of the diseased samples in type 2 diabetes and diabetes-associated cardiovascular diseased patients. Altered levels of cytoprotective enzymes were shown by decreased catalase activity, increased glutathione reductase activity and unaltered superoxide dismutase activity. Peroxidative activity of diseased hemoglobin was much higher compared to healthy controls indicating possible structural changes in pathologic hemoglobin molecule as a result of disease induced oxidative stress. This result is in good agreement with the observation that thermal stability of pathologic hemoglobin was also found to be less compared to control subjects. Enhanced oxygen releasing capacity of tetrameric oxyhemoglobin was monitored in presence of the drug Trifluoperazine in pathologic red blood cells, maximum increment being noticed in diabetic cardiovascular diseased subjects. Conclusion: Hyperglycemia-induced oxidative stress was responsible to affect the thermal stability and oxygen releasing capacity of hemoglobin and the effect is more pronounced in diabetes-associated cardiovascular disease.
AB - Background: Macrovascular disease, especially cardiovascular accounts for most of the mortality in patients with type 2 diabetes mellitus. We compared oxidative stress, thermal stability and oxygen releasing capacity of hemoglobin in patients with type 2 diabetes mellitus and diabetes-associated cardiovascular disease. Methods: The study was performed on 38 control subjects, 31 diabetics, 36 diabetics with cardiovascular complications, and 33 non-diabetic cardiovascular subjects. Results: Enhanced oxidative stress was shown by an increased protein carbonyl content observed both in plasma and in hemolysate of the diseased samples in type 2 diabetes and diabetes-associated cardiovascular diseased patients. Altered levels of cytoprotective enzymes were shown by decreased catalase activity, increased glutathione reductase activity and unaltered superoxide dismutase activity. Peroxidative activity of diseased hemoglobin was much higher compared to healthy controls indicating possible structural changes in pathologic hemoglobin molecule as a result of disease induced oxidative stress. This result is in good agreement with the observation that thermal stability of pathologic hemoglobin was also found to be less compared to control subjects. Enhanced oxygen releasing capacity of tetrameric oxyhemoglobin was monitored in presence of the drug Trifluoperazine in pathologic red blood cells, maximum increment being noticed in diabetic cardiovascular diseased subjects. Conclusion: Hyperglycemia-induced oxidative stress was responsible to affect the thermal stability and oxygen releasing capacity of hemoglobin and the effect is more pronounced in diabetes-associated cardiovascular disease.
KW - Antioxidant enzymes
KW - Atherosclerosis
KW - Hyperglycemia
KW - Oxygen release
KW - Protein carbonyl content
KW - Thermal stability
UR - http://www.scopus.com/inward/record.url?scp=25644439968&partnerID=8YFLogxK
U2 - 10.1016/j.cccn.2005.05.018
DO - 10.1016/j.cccn.2005.05.018
M3 - Article
C2 - 16098498
AN - SCOPUS:25644439968
SN - 0009-8981
VL - 361
SP - 141
EP - 149
JO - Clinica Chimica Acta
JF - Clinica Chimica Acta
IS - 1-2
ER -