Investigations on the correlation of advanced glycated end products (AGE) associated fluorescence with blood glucose and oxidative stress in ethanol-administered diabetic rats

被引:9
作者
Gopal, V. Renju [1 ]
Indira, M. [1 ]
机构
[1] Univ Kerala, Dept Biochem, Thiruvananthapuram 695581, Kerala, India
关键词
Ethanol; Hyperglycemia; Advanced glycated end products; Malondialdehyde; Oxidative stress; NITRIC-OXIDE; MALONDIALDEHYDE; ACETALDEHYDE; MELLITUS; LIVER;
D O I
10.1016/j.etp.2009.03.004
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Diabetes mellitus and alcoholism are two well-known agents causing pathological complications in the body. Both cause oxidative stress and derangements in glucose homeostasis. Advanced glycated end products (AGEs) are formed in hyperglycemia and call cause pathological changes. In this Study, we investigated the relationship between AGE-associated fluorescence, in serum, tail tendon collagen, and eye lens with blood glucose and serum malondialdehyde (MDA) in alcohol administered diabetic rats. Blood glucose and glycated hemoglobin (HbA(1)C) decreased in ethanol-administered diabetic rats. Elevated AGE-associated fluorescence in serum, eye lens and tail tendon collagen were observed in alcoholic diabetic rats in spite of the reduced blood glucose levels compared to other groups. AGE-associated fluorescence correlated positively with serum MDA than with blood glucose. Up-regulation of the nuclear translocation of NF kappa B was more profound in the ethanol-administered diabetic group indicating the development of pathological complications. This indicates that the toxicity induced by diabetes has been potentiated in alcohol administered diabetic rats. Our histopathological studies also reinforce our findings. Hence serum AGE-linked fluorescence has the potential to be developed as a Surrogate biomarker for oxidative Stress. (C) 2009 Elsevier GmbH. All rights reserved.
引用
收藏
页码:157 / 162
页数:6
相关论文
共 23 条
[1]   Inhibition of advanced glycation endproduct formation by acetaldehyde: Role in the cardioprotective effect of ethanol [J].
Al-Abed, Y ;
Mitsuhashi, T ;
Li, HW ;
Lawson, JA ;
FitzGerald, GA ;
Founds, H ;
Donnelly, T ;
Cerami, A ;
Ulrich, P ;
Bucala, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (05) :2385-2390
[2]  
[Anonymous], UFAW HDB CARE MANAGE
[3]  
BADAWY AAB, 1977, ALCOHOL ALCOHOLISM, V12, P120
[4]  
BIRD RP, 1984, METHOD ENZYMOL, V105, P299
[5]  
COLLINS T, 1993, LAB INVEST, V68, P499
[6]   BCL-2 expression or antioxidants prevent hyperglycemia-induced formation of intracellular advanced glycation endproducts in bovine endothelial cells [J].
Giardino, I ;
Edelstein, D ;
Brownlee, M .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (06) :1422-1428
[7]   Insufficient glycemic control increases nuclear factor-κB binding activity in peripheral blood mononuclear cells isolated from patients with type I diabetes [J].
Hofmann, MA ;
Schiekofer, S ;
Kanitz, M ;
Klevesath, MS ;
Joswig, M ;
Lee, V ;
Morcos, M ;
Tritschler, H ;
Ziegler, R ;
Wahl, P ;
Bierhaus, A ;
Nawroth, PP .
DIABETES CARE, 1998, 21 (08) :1310-1316
[8]   Ethanol acutely stimulates islet blood flow, amplifies insulin secretion, and induces hypoglycemia via nitric oxide and vagally mediated mechanisms [J].
Huang, Zhen ;
Sjoeholm, Ake .
ENDOCRINOLOGY, 2008, 149 (01) :232-236
[9]   Advanced glycation end-products in patients with chronic alcohol misuse [J].
Kalousova, M ;
Zima, T ;
Popov, P ;
Spacek, P ;
Braun, M ;
Soukupova, J ;
Pelinkova, K ;
Kientsch-Engel, R .
ALCOHOL AND ALCOHOLISM, 2004, 39 (04) :316-320
[10]   CORRELATION OF GLUCOSE REGULATION AND HEMOGLOBIN-A-IC IN DIABETES-MELLITUS [J].
KOENIG, RJ ;
PETERSON, CM ;
JONES, RL ;
SAUDEK, C ;
LEHRMAN, M ;
CERAMI, A .
NEW ENGLAND JOURNAL OF MEDICINE, 1976, 295 (08) :417-425