The glutathione levels are reduced in Goto-Kakizaki rat retina, but are not influenced by aminoguanidine treatment

被引:19
作者
Agardh, CD [1 ]
Agardh, E
Hultberg, B
Qian, YN
Östenson, CG
机构
[1] Univ Lund Hosp, Dept Ophthalmol, S-22185 Lund, Sweden
[2] Univ Lund Hosp, Dept Internal Med, S-22185 Lund, Sweden
[3] Univ Lund Hosp, Dept Clin Chem, S-22185 Lund, Sweden
[4] Karolinska Hosp, Dept Endocrinol & Diabetol, S-10401 Stockholm, Sweden
关键词
aminoguanidine; diabetes mellitus; glutathione; Goto-Kakizaki (GK) rat; pericyte; retina;
D O I
10.1076/ceyr.17.3.251.5217
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Purpose. To examine the levels of the free radical protecting enzyme glutathione and the endothelial/pericyte ratio in retinal capillaries in the Goto-Kakizaki (GK) Wistar rat, with and without aminoguanidine treatment. Methods. Eight-month-old GK rats, with non-obese, spontaneous non-insulin-dependent diabetes mellitus (NIDDM), were examined after a six month period of aminoguanidine treatment. Glutathione levels were measured with high performance liquid chromatography and the endothelial/pericyte ratio was calculated in trypsin digested vessel preparations. Results. The levels of glutathione in GK rat retina were significantly lower compared to controls (p = 0.0108). There was no difference in the endothelial/pericyte ratio compared to matched control rats (1.8 +/- 0.2 vs. 1.8 +/- 0.1, respectively). Aminoguanidine treatment did not influence either the degree of hyperglycemia, the levels of glutathione or the endothelial/pericyte ratio in GK or control rat retina. Conclusions. The results indicate that impaired glucose metabolism may influence one of the defense mechanisms for oxidative stress, but also suggest that decreased glutathione levels occur prior to morphological signs of pericyte loss and/or endothelial cell proliferation in this animal model of hereditary NIDDM.
引用
收藏
页码:251 / 256
页数:6
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