Effects of BSO and NAC on glutathione metabolism, lipid peroxidation, and acentylcholinesterase activity in the brain of fenthion exposed Oreochromis niloticus

ABSTRACTMSc THESISEFFECTS of BSO and NAC on GLUTATHIONE METABOLISM, LIPIDPEROXIDATION, and ACETYLCHOLINESTERASE ACTIVITY in theBRAIN of FENTHION EXPOSED Oreochromis niloticusPetek PİNERUNIVERSITY of ÇUKUROVAINSTITUTE of NATURAL and APPLIED SCIENCESDEPARTMENT of BIOLOGYSupervisor: Prof. Dr. Nevin ÜNERYear : 2005, Page: 112Jury : Prof. Dr. Nevin ÜNER: Prof. Dr. Cahit ERDEM: Assoc. Prof. Dr. Bedii CİCİKThe aim of this study was to investigate the effects of buthionine sulfoximine (BSO)(50 mg/kg), a GSH synthesis inhibitor, and N-acetylcysteine (NAC) (100 mg/kg), anantioxidant and GSH precursor, on GSH and GSH-related enzymes, lipid peroxidation andon AChE enzyme activities in the brain of organophosphate fenthion exposed juvenileOreochromis niloticus. Animals were left in fenthion solutions over 24, 48 and 96 h periodsand at end of each period GSH and GSSG levels, GSH/GSSG ratio, GPx, GR, GST, γ-GT, γ-GCS enzyme activities were determined to evaluate the effects of BSO and NAC on GSHsystem, MDA contents were determined to find out their effects on lipid peroxidation andAChE enzyme activity was determined to study their neurotoxic effects. All measurementswere carried out using spectrophotometric methods. The applied 20% LC50 fenthionconcentration (0.45 ppm) was determined through a LC50 study carried out according toAPHA norms. The same procedure was repeated after 24, 48 and 96 h depuration periods.Fenthion increased the GSH/GSSG ratio, GSSG level and GPx activity in exposureperiods. Treatment with BSO decreased the GSH/GSSG ratio, GSH levels and GR activity,while increasing GSSG levels, GPx and γ-GT activities in the brain of fenthion exposed fish.NAC, which was applied at a higher dose, decreased GSH levels and GPx activity, howeverelevated GSH/GSSG ratio and GST activity. No lipid peroxidation was observed in anyexperimental group compared with the controls. AChE activities showed a decrease in allfenthion treated fish. BSO and NAC were elevated AChE activity.Glutathione and GSH-related enzymes had a role in fenthion toxicity. Fenthion withBSO application increased the toxic effects. NAC caused oxidative stress in its presentconcentration. γ-GCS activity could not be determined in the brain of O. niloticus. It wasfirst shown by the present study that BSO and NAC increase the AChE activity in brain.Four depuration days were not found sufficient for the elimination of determined effects inbrain.Key Words: Fish, Fenthion, N-acetylcysteine, Buthionine sulfoximine, GlutathioneII