Ovarian toxicity of cyclophosphamide alone and in combination with ovarian irradiation in the rat.
The effects of radiation and chemotherapy on gonadal function are relevant to the morbidity induced by such treatments. Cyclophosphamide given i.p. to rats on Day 30 of age delayed vaginal opening, prevented vaginal cyclicity, and caused a reduction in serum estradiol and progesterone. Antral follicular atresia increased in a dose-dependent fashion in response to cyclophosphamide (0 mg/kg, 53.5%; 1 mg/kg, 67.3%; 50 mg/kg, 65.7%; 100 mg/kg, 73.9%; 150 mg/kg, 92.2%). Despite such alterations in ovarian function, serum gonadotrophins did not rise. The concurrent administration of 0, 20, 30, 40, 50, and 60 Gy of radiation to the exteriorized ovaries in rats receiving 50 mg/kg cyclophosphamide induced widespread loss of primordial, preantral, and healthy antral follicles associated with reduction in serum progesterone and estradiol. Such irradiation induced dose-related increases in serum follicle-stimulating hormone and luteinizing hormone. Parenteral cyclophosphamide and local irradiation appear to induce ovarian toxicity by different mechanisms.
D000818:Animals; D003520:Cyclophosphamide / Q000633:toxicity*; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D005496:Follicular Atresia / Q000187:drug effects; D007986:Luteinizing Hormone / Q000097:blood; D010053:Ovary / Q000187:drug effects* / Q000528:radiation effects; D011374:Progesterone / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains
D011374:Progesterone; D004958:Estradiol; D003520:Cyclophosphamide; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone