title: Antioxidant potential of fungal metabolite nigerloxin during eye lens abnormalities in galactose-fed rats.
abstract: BACKGROUND
  The role of osmotic and oxidative stress has been strongly implicated in the pathogenesis of cataract. Nigerloxin, a fungal metabolite, has been shown to possess aldose reductase inhibition and improved antioxidant defense system in lens of diabetic rats. In the present study, the beneficial influence of nigerloxin was investigated in galactose-induced cataract in experimental animals.
  
  
  METHODS
  Cataract was induced in Wistar rats by feeding 30% galactose in diet. Groups of galactose-fed rats were orally administered with nigerloxin (25 and 100 mg/kg body weight/day) for 24 days.
  
  
  RESULTS
  Lens aldose reductase activity was increased significantly in galactose-fed animals. Lens lipid peroxides and advanced glycation end products were also significantly increased. Antioxidant molecule - reduced glutathione, total thiols and activities of antioxidant enzymes superoxide dismutase and glutathione peroxidase were decreased in the lens of galactose-fed animals. Oral administration of nigerloxin once a day for 24 days at a dose of 100 mg/kg body weight, significantly decreased lens lipid peroxides and advanced glycation end products in galactose-fed rats. Lens aldose reductase activity was reduced and lens antioxidant molecules and antioxidant enzyme activities were elevated significantly by nigerloxin administration.
  
  
  CONCLUSIONS
  The results suggest that alteration in polyol pathway and antioxidant defense system were countered by nigerloxin in the lens of galactose-fed animals, suggesting the potential of nigerloxin in ameliorating the development of galactose-induced cataract in experimental animals.
authors.affiliation: Department of Biochemistry and Nutrition, CSIR's Central Food Technological Research Institute, Mysore, India.
authors.forename: Bharathinagar S
authors.initials: BS
authors.lastname: Suresha
authors.forename: Krishnapura
authors.initials: K
authors.lastname: Srinivasan
mesh_terms: D000449:Aldehyde Reductase / Q000037:antagonists & inhibitors; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001234:Aspergillus niger / Q000737:chemistry; D001565:Benzoates / Q000494:pharmacology*; D002386:Cataract / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D005690:Galactose / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D007908:Lens, Crystalline / Q000187:drug effects* / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D011108:Polymers / Q000378:metabolism; D011407:Propane / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013438:Sulfhydryl Compounds / Q000378:metabolism; D014364:Tryptophan / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001565:Benzoates; D011108:Polymers; D013438:Sulfhydryl Compounds; C469528:nigerloxin; C024617:polyol; D014364:Tryptophan; D000449:Aldehyde Reductase; D005978:Glutathione; D011407:Propane; D005690:Galactose