Regulation of ovarian antioxidant vitamins, reduced glutathione, and lipid peroxidation by luteinizing hormone and prostaglandin F2 alpha.
Reactive oxygen species are generated by the rat ovary, and they evoke marked antigonadotropic responses in ovarian cells. Protection against reactive oxygen species is provided by antioxidants such as vitamins C, E, and A, and reduced glutathione (GSH). Our objectives were to establish the ovarian levels of these antioxidants during development and regression of the corpus luteum of the pseudopregnant rat and to determine whether these levels were changed by an acute treatment with either a luteotropic (LH) or luteolytic (prostaglandin [PG] F2 alpha) agent. In addition, we evaluated the extent of oxidative activity in the ovary by determining the level of lipid peroxidation. Follicular development was associated with a significant increase in ovarian levels of vitamin A and GSH, whereas levels of vitamins E and C were unchanged. During the luteal phase, vitamin E levels tended to increase, whereas vitamin A and GSH levels decreased. Luteal regression was associated with a marked increase in ovarian levels of vitamins E and A, whereas GSH levels increased only transiently. Acute treatment with LH in the midluteal phase produced a transient decrease in vitamin C levels that was maximal at 4 h. Luteal vitamin E levels were markedly increased 24 h after LH treatment, whereas vitamin A levels were unchanged, and no evidence of lipid peroxidation was seen. Acute treatment with PGF2 alpha produced a transient decrease in luteal vitamin C levels coincident with transient lipid peroxidation and a sustained fall in serum progesterone levels. Ovarian vitamin A levels were elevated 24 h after PGF2 alpha treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Aten
R F
RF
Department of Ob/Gyn, Yale University School of Medicine, New Haven, Connecticut 06510.
Duarte
K M
KM
Behrman
H R
HR
D000818:Animals; D000975:Antioxidants; D001205:Ascorbic Acid / Q000378:metabolism; D003338:Corpus Luteum / Q000502:physiology; D015237:Dinoprost / Q000494:pharmacology*; D005260:Female; D005978:Glutathione / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000187:drug effects*; D007986:Luteinizing Hormone / Q000494:pharmacology*; D003341:Luteolysis / Q000502:physiology; D010053:Ovary / Q000187:drug effects / Q000378:metabolism*; D010084:Oxidation-Reduction; D011555:Pseudopregnancy; D051381:Rats; D014801:Vitamin A / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism; D014815:Vitamins / Q000378:metabolism*
D000975:Antioxidants; D014815:Vitamins; D014801:Vitamin A; D014810:Vitamin E; D007986:Luteinizing Hormone; D015237:Dinoprost; D005978:Glutathione; D001205:Ascorbic Acid