title: Effect of I-deprenyl and gliclazide on oxidant stress/antioxidant status and dna damage in a diabetic rat model.
abstract: BACKGROUND
  This study investigates the possible effect of monoamine oxidase inhibitor (MAOI), selegyline (l-deprenyl), in combination with oral antidiabetic-gliclazide (OAD), in preventing oxidative stress in streptozotocin-induced diabetes model in male Swiss Albino rats by measuring oxidant stress/ DNA damage and antioxidant levels.
  
  
  METHODS
  Diabetic rats were divided into four groups (n = 10) as (1) diabetic untreated (DM), (2) deprenyl treated (DM + D), (3) gliclazide treated (DM + O), and (4) gliclazide and deprenyl treated (DM + O + D). Controls were divided into two groups (n = 8) (1) untreated (C), and (2) deprenyl treated (C + D). Gliclazide 5 mg/kg and/or MAOI 0.25 mg/kg daily were given orally by gavage for 4 weeks. At the end of the 12th week, catalase and superoxide dismutase (SOD) levels in erythrocyte lysates (EL); total antioxidant status (TAS), 8-hydroxy-deoxyguanosine (8-OHdG), malondialdehyde (MDA), and vitamin A and E levels in plasma, MDA, and MAO in liver homogenates were determined.
  
  
  RESULTS
  Diabetic rats showed a decrease in EL-SOD, plasma TAS, and vitamin E, and an increase in plasma 8-OHdG, plasma, and liver MDA levels (p < 0.05). Gliclazide and/or deprenyl decreased 8OHdG levels and increased antioxidant levels and survival when compared with untreated diabetic rats (p < 0.05). The lowest 8-OHdG levels were determined in the DM +O + D group.
  
  
  CONCLUSIONS
  The combined treatment of deprenyl and gliclazide may contribute to the control of the physiopathological mechanisms underlying both the process of aging and type 2 diabetes by reducing oxidant stress and DNA damage, improving antioxidant status, and increasing survival, and may have implications for further clinical studies.
authors.affiliation: Ege University Medical School, Department of Biochemistry, 35100 Bornova, Izmir, Turkey. galper@med.ege.edu.tr
authors.forename: Gulinnaz
authors.initials: G
authors.lastname: Alper
authors.forename: Seda
authors.initials: S
authors.lastname: Irer
authors.forename: Erdal
authors.initials: E
authors.lastname: Duman
authors.forename: Osman
authors.initials: O
authors.lastname: Caglayan
authors.forename: Candeger
authors.initials: C
authors.lastname: Yilmaz
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000375:Aging; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight / Q000187:drug effects; D004249:DNA Damage / Q000187:drug effects; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000503:physiopathology*; D004195:Disease Models, Animal; D005907:Gliclazide / Q000494:pharmacology*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008099:Liver / Q000737:chemistry; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000097:blood; D008995:Monoamine Oxidase / Q000378:metabolism; D008996:Monoamine Oxidase Inhibitors / Q000494:pharmacology*; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D012642:Selegiline / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000097:blood; D014801:Vitamin A / Q000097:blood; D014810:Vitamin E / Q000097:blood
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D008996:Monoamine Oxidase Inhibitors; D016877:Oxidants; D014801:Vitamin A; D014810:Vitamin E; D012642:Selegiline; D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D013482:Superoxide Dismutase; D008995:Monoamine Oxidase; D005907:Gliclazide; D003849:Deoxyguanosine