title: Protective role of chrysin against oxidative stress in d-galactose-induced aging in an experimental rat model.
abstract: OBJECTIVE
  To evaluate the putative protective role of chrysin, an isoflavone, on D-galactose-induced aging in an experimental rat model.
  
  
  METHODS
  Rats were divided into five groups of five each. Group I received 0.9% saline only. Groups II, III and IV received d-galactose (50 mg/kg bodyweight) intraperitoneally, additionally group III and group IV received chrysin (20 mg/kg bodyweight) and α-tocopherol acetate (200 mg/kg bodyweight), respectively. Group V received chrysin alone. The experiment period was for a period of 8 weeks. After the rats were killed, the tissue samples were analyzed for mean activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, glucose-6-phosphate dehydrogenase, reduced glutathione, vitamin C, vitamin E, malondialdehyde and protein carbonyl. Histopathological studies were also carried out for morphological conformation.
  
  
  RESULTS
  Tissue samples from D-galactose-exposed untreated rats showed significantly (P < 0.05) lower levels of enzymatic and non-enzymatic anti-oxidants, and significantly (P < 0.05) higher levels of malondialdehyde and protein carbonyl when compared with group I and group III rats. Oral administration of chrysin for a period of 8 weeks, concomitant with the exposure to D-galactose, appeared to protect against oxidative damage and maintained all parameters at near normal levels. Histopathological studies confirmed the oxidative damage caused by D-galactose alone in tissues and also showed the tissue protective role of chrysin in rats receiving D-galactose and chrysin.
  
  
  CONCLUSIONS
  These results suggest that chrysin protects against oxidative stress-induced tissue damage in D-galactose-induced aging in an experimental rat model.
authors.affiliation: Department of Animal Science, School of Life Sciences, Bharathidasan University             Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirappalli, India.
authors.forename: Kalaiselvi Velayutham
authors.initials: KV
authors.lastname: Anand
authors.forename: Mohamed Sultan
authors.initials: MS
authors.lastname: Mohamed Jaabir
authors.forename: Philip A
authors.initials: PA
authors.lastname: Thomas
authors.forename: Pitchairaj
authors.initials: P
authors.lastname: Geraldine
mesh_terms: D000375:Aging / Q000187:drug effects* / Q000378:metabolism*; D000704:Analysis of Variance; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005419:Flavonoids / Q000494:pharmacology*; D005690:Galactose / Q000378:metabolism*; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D005419:Flavonoids; C043561:chrysin; D008315:Malondialdehyde; D005954:Glucosephosphate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione; D001205:Ascorbic Acid; D005690:Galactose