REGULATION OF TOTAL OVARIAN GLUTATHIONE CONTENT IN THE RAT

Glutathione (GSH) is an important intracellular thiol capable of alter ing metabolism following exposure to certain important biologic toxica nts including radiation and cyclophosphamide. In order to evaluate the inhibition of glutathione synthesis in the ovary, 30-day-old Sprague Dawley rats were treated with either saline or 0.6-mu-mol/kg (0.133 mg /kg), 6.0-mu-mol/kg (1.33 mg/kg), or 4.5 mmol/kg (1000 mg/kg) buthioni ne sulphoximine (BSO) IP and sacrificed at 0, 1, 2, 4, 6, 8, and 24 h. There was an inhibition of glutathione synthesis with 4.5 mmol/kg (10 00 mg/kg) BSO with a nadir at 8 h (P < 0.001) and complete recovery at 24 h. In the subsequent experiments rats were divided into four group s. All animals received either saline or BSO 4.5 mmol/kg/day (1000 mg/ kg/day) from day 27 to 30 of life and either saline or PMSG 5 IU IP on day 29 of life. BSO reduced ovarian content of GSH (saline-saline com pared with BSO-saline, P < 0.0001), which was countered by the prior a dministration of PMSG (BSO-saline compared with BSO-PMSG, P < 0.005). Glutathione levels were as follows: saline-saline 4.3 +/- 0.04; saline -PMSG 5.0 +/- 0.4; BSO-saline 2.13 +/- 0.2; BSO-PMSG 3.24 +/- 0.2 nmol /mg ovary. These findings suggest the ovary is susceptible to GSH depl etion by in vivo administration of BSO. Gonadotropin (PMSG) is capable of effecting a partial return of total ovarian GSH content.