title: Melatonin ameliorates oxidative damage in hyperglycemia-induced liver injury.
abstract: OBJECTIVE
  Melatonin (N-acetyl-5-methoxy-tryptamine) is synthesized mainly by the pineal gland and its antioxidant properties have been demonstrated both in short and long term studies. Our aim was to clarify the effects of hyperglycemia and to administer melatonin on lipid peroxidation, protein oxidation and oxidative DNA damage in rat.
  
  
  METHODS
  Malondialdehyde (MDA), protein carbonyl (PCO) and total thiol (T-SH) levels were determined in plasma and liver tissue, glutathione (GSH) levels in erythrocyte and liver tissue, and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in plasma and liver. Thirty-eight male Wistar rats were divided into four groups: 1--injected with saline (n = 8), 2--injected with melatonin (n = 10), 3--injected with STZ (65 mg/kg, i.p.) (diabetic group) (n = 10) and 4--injected with melatonin (10 mg/kg/day, i.p.) and STZ (65 mg/kg, i.p.) (n = 10) for 8 weeks (diabetic+ melatonin group). Colorimetric methods were used to determine the level of the oxidative stress markers. 8-OhdGwas measured using ELISA.
  
  
  RESULTS
  MDA, PCO and 8-OHdG levels in the plasma and the liver homogenates of diabetic rats were higher than controls and were significantly reduced after melatonin treatment. T-SH and GSH levels in samples were markedly reduced in untreated diabetic rats compared with control rats; however, these parameters were increased in diabetic rats following melatonin treatment.
  
  
  CONCLUSIONS
  Our findings showed that melatonin administration partially ameliorated oxidative damage in liver injury in STZ-induced diabetic rats. The present study suggests that melatonin functions as a potent antioxidant agent in diabetes. Melatonin, a nutritional supplement, may be a good therapeutic option for diabetic patients.
authors.affiliation: Kirklareli University, School of Health, Kirklareli, Turkey.
authors.forename: Gulcan G
authors.initials: GG
authors.lastname: Korkmaz
authors.forename: Hafize
authors.initials: H
authors.lastname: Uzun
authors.forename: Ufuk
authors.initials: U
authors.lastname: Cakatay
authors.forename: Seval
authors.initials: S
authors.lastname: Aydin
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001835:Body Weight; D004249:DNA Damage; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005786:Gene Expression Regulation; D005978:Glutathione / Q000378:metabolism; D006943:Hyperglycemia / Q000378:metabolism*; D015227:Lipid Peroxidation; D008099:Liver / Q000293:injuries* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008550:Melatonin / Q000378:metabolism*; D018384:Oxidative Stress; D010100:Oxygen / Q000737:chemistry; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D013438:Sulfhydryl Compounds; D008315:Malondialdehyde; D013311:Streptozocin; D005978:Glutathione; D008550:Melatonin; D010100:Oxygen