Characterization of oxidative stress in various tissues of diabetic and galactose-fed rats

R. M. Strother, T. G. Thomas, M. Otsyula, R. A. Sanders, J. B. Watkins

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Rats fed a galactose-rich diet have been used for several years as a model for diabetes to study, particularly in the eye, the effects of excess blood hexoses. This study sought to determine the utility of galactosemia as a model for oxidative stress in extraocular tissues by examining biomarkers of oxidative stress in galactose-fed rats and experimentally-induced diabetic rats. Sprague-Dawley rats were divided into four groups: experimental control; streptozotocin-induced diabetic; insulin-treated diabetic; and galactose-fed. The rats were maintained on these regimens for 30 days, at which point the activities of catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase, as well as levels of lipid peroxidation and reduced and oxidized glutathione were determined in heart, liver, and kidney. This study indicates that while there are some similarities between galactosemic and diabetic rats in these measured indices of oxidative stress (hepatic catalase activity levels and hepatic and renal levels of oxidized glutathione in both diabetic and galactosemic rats were significantly decreased when compared to normal), overall the galactosemic rat model is not closely parallel to the diabetic rat model in extra-ocular tissues. In addition, several effects of diabetes (increased hepatic glutathione peroxidase activity, increased superoxide dismutase activity in kidney and heart, decreased renal and increased cardiac catalase activity) were not mimicked in galactosemic rats, and glutathione concentration in both liver and heart was affected in opposite ways in diabetic rats and galactose-fed rats. Insulin treatment reversed/prevented the activity changes in renal and cardiac superoxide dismutase, renal and cardiac catalase, and hepatic glutathione peroxidase as well as the hepatic changes in lipid peroxidation and reduced and oxidized glutathione, and the increase in cardiac glutathione. Thus, prudence should be exercised in the use of experimentally galactosemic rats as a model for diabetes until the correspondence of the models has been more fully characterized.

Original languageEnglish
Pages (from-to)211-216
Number of pages6
JournalInternational Journal of Experimental Diabetes Research
Volume2
Issue number3
StatePublished - 2001

Fingerprint

Galactose
Oxidative Stress
Liver
Kidney
Catalase
Glutathione
Glutathione Disulfide
Glutathione Peroxidase
Superoxide Dismutase
Lipid Peroxidation
Insulin
Galactosemias
Hexoses
Glutathione Reductase
Streptozocin
Sprague Dawley Rats
Biomarkers
Diet
Control Groups

Keywords

  • Diabetes
  • Galactose
  • Galactosemia
  • Glucose
  • Rat
  • Streptozotocin

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Medicine(all)

Cite this

Strother, R. M., Thomas, T. G., Otsyula, M., Sanders, R. A., & Watkins, J. B. (2001). Characterization of oxidative stress in various tissues of diabetic and galactose-fed rats. International Journal of Experimental Diabetes Research, 2(3), 211-216.

Characterization of oxidative stress in various tissues of diabetic and galactose-fed rats. / Strother, R. M.; Thomas, T. G.; Otsyula, M.; Sanders, R. A.; Watkins, J. B.

In: International Journal of Experimental Diabetes Research, Vol. 2, No. 3, 2001, p. 211-216.

Research output: Contribution to journalArticle

Strother, RM, Thomas, TG, Otsyula, M, Sanders, RA & Watkins, JB 2001, 'Characterization of oxidative stress in various tissues of diabetic and galactose-fed rats', International Journal of Experimental Diabetes Research, vol. 2, no. 3, pp. 211-216.
Strother, R. M. ; Thomas, T. G. ; Otsyula, M. ; Sanders, R. A. ; Watkins, J. B. / Characterization of oxidative stress in various tissues of diabetic and galactose-fed rats. In: International Journal of Experimental Diabetes Research. 2001 ; Vol. 2, No. 3. pp. 211-216.
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