Oxidative stress in rats after 60 days of hypergalactosemia or hyperglycemia.
Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosylated hemoglobin A(1c) concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.
Otsyula
Mary
M
College of Health Sciences, Moi University, Eldoret, Kenya.
King
Matthew S
MS
Ketcham
Tonya G
TG
Sanders
Ruth A
RA
Watkins
John B
JB
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002374:Catalase / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D004032:Diet; D004195:Disease Models, Animal; D005690:Galactose / Q000008:administration & dosage; D005693:Galactosemias / Q000378:metabolism* / Q000473:pathology; D005979:Glutathione Peroxidase / Q000378:metabolism; D006442:Glycated Hemoglobin / Q000032:analysis; D006321:Heart / Q000187:drug effects; D006943:Hyperglycemia / Q000378:metabolism* / Q000473:pathology; D007328:Insulin / Q000627:therapeutic use; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D001786:Blood Glucose; D002374:Catalase; D005690:Galactose; D005979:Glutathione Peroxidase; D006442:Glycated Hemoglobin; D007328:Insulin; D013482:Superoxide Dismutase; D017392:Thiobarbituric Acid Reactive Substances