TY - JOUR
T1 - Increased hepatic lipid soluble antioxidant capacity as compared to other organs of streptozotocin-induced diabetic rats
T2 - A cyclic voltammetry study
AU - Elangovan, V.
AU - Shohami, E.
AU - Gati, I.
AU - Kohen, R.
PY - 2000
Y1 - 2000
N2 - It has been suggested that oxidative stress plays an important role in the chronic complications of diabetes. The experimental findings regarding the changes in tissue antioxidant enzymes and lipid peroxidation of diabetic tissues have been inconsistent. Previous studies in our laboratory demonstrated that the reducing power of a specific tissue correlates with its low molecular weight antioxidant (LMWA) capacity. In the present study, the overall LMWA capacity (reducing equivalents) of plasma and tissues of streptozotocin (STZ)-induced diabetic rats (1-4 weeks) and insulin treated diabetic rats were measured by cyclic voltammetry. Levels of water and lipid soluble LMWA capacity progressively decreased in the diabetic plasma, kidney, heart and brain, while the diabetic liver, at 2, 3 and 4 weeks after STZ injection, showed a significant increase in the overall lipid soluble LMWA capacity (p<0.001). Subsequently, analysis of specific components by high pressure liquid chromatography (electrochemical detection) showed decreased levels of ascorbic acid in plasma, kidney, heart and brain of diabetic animals. The α-tocopherol level dropped in all tissues, except for the liver in which there was a significant increase (p<0.01 and p<0.001 at 2-4 weeks). Lipid peroxidation was assessed by conjugated diene levels, which increased significantly in all diabetic tissues except the liver. Insulin treatment that was started after 3 weeks of diabetes and continued for 3 weeks showed no change in the conjugated dienes and in the overall LMWA capacity in all organs. Our results suggest a unique behavior of the liver in the STZ-induced diabetic rats to the stress and indicate its higher capacity to cope with oxidative stress as compared to other organs.
AB - It has been suggested that oxidative stress plays an important role in the chronic complications of diabetes. The experimental findings regarding the changes in tissue antioxidant enzymes and lipid peroxidation of diabetic tissues have been inconsistent. Previous studies in our laboratory demonstrated that the reducing power of a specific tissue correlates with its low molecular weight antioxidant (LMWA) capacity. In the present study, the overall LMWA capacity (reducing equivalents) of plasma and tissues of streptozotocin (STZ)-induced diabetic rats (1-4 weeks) and insulin treated diabetic rats were measured by cyclic voltammetry. Levels of water and lipid soluble LMWA capacity progressively decreased in the diabetic plasma, kidney, heart and brain, while the diabetic liver, at 2, 3 and 4 weeks after STZ injection, showed a significant increase in the overall lipid soluble LMWA capacity (p<0.001). Subsequently, analysis of specific components by high pressure liquid chromatography (electrochemical detection) showed decreased levels of ascorbic acid in plasma, kidney, heart and brain of diabetic animals. The α-tocopherol level dropped in all tissues, except for the liver in which there was a significant increase (p<0.01 and p<0.001 at 2-4 weeks). Lipid peroxidation was assessed by conjugated diene levels, which increased significantly in all diabetic tissues except the liver. Insulin treatment that was started after 3 weeks of diabetes and continued for 3 weeks showed no change in the conjugated dienes and in the overall LMWA capacity in all organs. Our results suggest a unique behavior of the liver in the STZ-induced diabetic rats to the stress and indicate its higher capacity to cope with oxidative stress as compared to other organs.
KW - Cyclic voltammetry
KW - Liver
KW - Low molecular weight antioxidant capacity
KW - Oxidative stress
KW - Reducing equivalents
KW - Vitamin C
KW - α-tocopherol
UR - http://www.scopus.com/inward/record.url?scp=0033959052&partnerID=8YFLogxK
U2 - 10.1080/10715760000300131
DO - 10.1080/10715760000300131
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
C2 - 10653483
AN - SCOPUS:0033959052
SN - 1071-5762
VL - 32
SP - 125
EP - 134
JO - Free Radical Research
JF - Free Radical Research
IS - 2
ER -
