R. Kakkar et al., INCREASED OXIDATIVE STRESS IN RAT-LIVER AND PANCREAS DURING PROGRESSION OF STREPTOZOTOCIN-INDUCED DIABETES, Clinical science, 94(6), 1998, pp. 623-632
1. Oxygen free radicals have been suggested to be a contributory facto
r in complications of diabetes mellitus. There are many reports indica
ting the changes in parameters of oxidative stress in diabetes mellitu
s, In this study we aimed to identify whether oxidative stress occurs
in the liver and pancreas in the initial stages of development of diab
etes. 2. We therefore investigated the lipid peroxide level (thiobarbi
turic acid-reactive substances, TEARS) and activities of antioxidant e
nzymes [superoxide dismutase (SOD), catalase and glutathione peroxidas
e] in liver and pancreas of control and streptozotocin-induced diabeti
c rats at various stages of development of diabetes. 3. Male Sprague-D
awley rats were divided into two groups: group I, control (n = 42) and
group II, diabetic (II = 42), Each group was further subdivided into
seven groups consisting of six rats each. Rats in these subgroups were
studied at weekly intervals (0 to 6 weeks). Plasma glucose levels, TE
ARS levels and activities of antioxidant enzymes were measured in live
r and pancreas at various time intervals. 4. There was a significant (
P < 0.05) and progressive increase in TEARS levels of liver and pancre
as in the diabetic group. Total SOD and Cu-Zn-SOD activity increased (
P < 0.05) with progression of diabetes while Mn-SOD activity showed no
significant change in either tissue. Catalase and glutathione peroxid
ase activities increased significantly (P < 0.05) in liver and pancrea
s, 5. Immunohistochemical study of pancreatic islet revealed a decreas
e in the expression of insulin with progression of diabetes. However,
glucagon and somatostatin showed an increase in immunoreactivity and a
difference in their distribution pattern. 6. The findings of the pres
ent study suggest that oxidative stress starts at early onset of diabe
tes mellitus and increases progressively. In conclusion, the structura
l damage to these tissues or complications of diabetes mellitus may be
due to oxidative stress.