title: Decrease in mitochondrial oxidative protein damage parameters in the streptozotocin-diabetic rat.
abstract: BACKGROUND
  Many authors have shown that hyperglycemia leads to an increase in oxidative protein damage in diabetes. The aim of this study was to reveal the susceptibility of mitochondria from liver, pancreas, kidney, and skeletal muscle of diabetic Sprague-Dawley rats, a model of type 1 diabetes, to oxidative protein damage.
  
  
  METHODS
  Mitochondrial fractions were obtained by differential centrifugation. To show the effect of hyperglycemia in promoting oxidative protein damage, we determined mitochondrial protein carbonyl, total thiol, nitrotyrosine, advanced oxidation protein products, and lipid hydroperoxide levels. The levels of the studied markers, except nitrotyrosine, were determined by colorimetric methods. Nitrotyrosine levels were measured by ELISA. All values were compared with those of the controls by using the Mann-Whitney U-test.
  
  
  RESULTS
  Nitrotyrosine and lipid hydroperoxide levels were decreased and other parameters were not changed in liver mitochondria of diabetic rats. Protein carbonyl, nitrotyrosine, advanced oxidation protein products, and lipid hydroperoxide levels were decreased and total thiol levels were not changed in pancreas mitochondria of diabetic rats. Only advanced oxidation protein products and lipid hydroperoxide levels were decreased in kidney mitochondria of diabetic rats. The levels of the same parameters were not significantly different in muscle mitochondria of diabetic rats.
  
  
  CONCLUSIONS
  The decrease in mitochondrial oxidative protein damage in diabetes may correspond to either an increase in antioxidant defense mechanisms or a different adaptive response of the cells to the increased extramitochondrial oxidative stress in diabetes. The mitochondrial oxidative protein damage-lowering mechanisms in diabetes remain to be clarified.
authors.affiliation: Istanbul University, Cerrahpaşa Faculty of Medicine, Department of Biochemistry, Istanbul, Turkey.
authors.forename: Refik
authors.initials: R
authors.lastname: Kayali
authors.forename: Ufuk
authors.initials: U
authors.lastname: Cakatay
authors.forename: Ayşegül
authors.initials: A
authors.lastname: Telci
authors.forename: Tülay
authors.initials: T
authors.lastname: Akçay
authors.forename: Ahmet
authors.initials: A
authors.lastname: Sivas
authors.forename: Tuncay
authors.initials: T
authors.lastname: Altug
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism; D004195:Disease Models, Animal; D007668:Kidney / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010179:Pancreas / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013438:Sulfhydryl Compounds / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000032:analysis
chemical_list: D008054:Lipid Peroxides; D013438:Sulfhydryl Compounds; C002744:3-nitrotyrosine; D014443:Tyrosine