Document Detail

Regulation of lipid peroxidation by nitric oxide and PGF2alpha during luteal regression in rats.
MedLine Citation:
PMID:  11277883     Owner:  NLM     Status:  MEDLINE    
Corpus luteum regression is related to an increased generation of reactive oxygen species. Although several studies indicate that PGF(2alpha) is involved in regression of the corpus luteum in mammalian species through an increase in reactive oxygen species, the exact mechanism remains unknown. In the present study, the relationship between nitric oxide and PGF(2alpha) in regulation of lipid peroxidation was studied. Ovarian tissue from pseudopregnant rats at mid- (day 5) or late phase or at the time of regression (day 9 of pseudopregnancy) of corpus luteum development was used. Thiobarbituric acid reactants, used as a lipid peroxidation index, were higher on day 9 of pseudopregnancy than on day 5. In contrast, glutathione content (an antioxidant metabolite) was lower on day 9 than on day 5 of pseudopregnancy. These results indicate that there was an enhanced oxidative status in ovarian tissue during luteolysis. Administration of N(omega)-nitro-L-arginine methyl ester (L-NAME: 600 micromol l(-1)), a competitive nitric oxide synthase (NOS) inhibitor, led to a decrease in basal thiobarbituric acid reactant content in ovarian tissue from rats on day 9 of pseudopregnancy only, indicating that during regression of the corpus luteum, NO could act as intermediary in ovarian lipid peroxidation. Administration of a luteolytic dose (3 microg kg(-1) body weight i.p.) of a synthetic PGF(2alpha) increased thiobarbituric acid reactant content in ovaries from rats on day 9 of pseudopregnancy. As this effect was reversed partially by L-NAME, it is proposed that during regression of corpora lutea, PGF(2alpha) and NO are involved in regulation of lipid peroxidation. As this effect was only reversed partially, it is possible that there is another mechanism involving PGF(2alpha) (but not the NO-NOS pathway) in regulation of ovarian lipid peroxidation. Furthermore, the administration of PGF(2alpha) enhanced ovarian NOS activity, whereas cyclooxygenase inhibition (by indomethacin treatment in vivo) reduced it. As western blotting of ovarian homogenates obtained from PGF(2alpha)-injected rats increased inducible NOS (iNOS) content, it is concluded that PGF(2alpha) enhances both activity and synthesis of NO in rat ovarian tissues during luteolysis. Taken together, these results indicate that in ovaries with regressing corpora lutea, both NO and PGF(2alpha) are involved in part in regulation of lipid peroxidation.
A B Motta; A Estevez; A Franchi; S Perez-Martinez; M Farina; M L Ribeiro; A Lasserre; M F Gimeno
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Reproduction (Cambridge, England)     Volume:  121     ISSN:  1470-1626     ISO Abbreviation:  Reproduction     Publication Date:  2001 Apr 
Date Detail:
Created Date:  2001-03-30     Completed Date:  2001-07-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100966036     Medline TA:  Reproduction     Country:  England    
Other Details:
Languages:  eng     Pagination:  631-7     Citation Subset:  IM    
Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Consejo de Investigaciones Científicas y Técnicas (CONICET), Serrano 669, (1414) Buenos Aires, Argentina.
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MeSH Terms
Blotting, Western
Cyclooxygenase Inhibitors / pharmacology
Dinoprost / pharmacology*
Enzyme Inhibitors / pharmacology
Glutathione / analysis
Indomethacin / pharmacology
Lipid Peroxidation / drug effects*
Luteolysis / physiology*
Models, Animal
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / pharmacology*
Nitric Oxide Synthase / antagonists & inhibitors
Ovary / drug effects,  metabolism*
Rats, Wistar
Thiobarbituric Acid Reactive Substances / analysis
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Enzyme Inhibitors; 0/Thiobarbituric Acid Reactive Substances; 10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; 53-86-1/Indomethacin; 551-11-1/Dinoprost; 70-18-8/Glutathione; EC Oxide Synthase

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