Biochemical changes in rat endometrium induced by oestrogens

The effect of oestradiol (Oe2) or ethinyloestradiol (EOe) on several enzymes, soluble protein and DNA in the endometrium was studied in ovariectomized adult rats. The most marked effect of Oe2 was the increase in the activity of lactate dehydrogenase (LDH). If the treatment was started on the day of...

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Published inActa endocrinologica (Copenhagen) Vol. 96; no. 3; pp. 382 - 388
Main Authors Jelínková, M, Jelínek, J, van der Vies, J
Format Journal Article
LanguageEnglish
Published Denmark 01.03.1981
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Summary:The effect of oestradiol (Oe2) or ethinyloestradiol (EOe) on several enzymes, soluble protein and DNA in the endometrium was studied in ovariectomized adult rats. The most marked effect of Oe2 was the increase in the activity of lactate dehydrogenase (LDH). If the treatment was started on the day of ovariectomy, it took approximately 8 days to reach a constant elevation. If the administration of Oe2 was started one week after castration, the maximum response was seen after 4 days of treatment. Using the latter schedule a linear dose-reponse regression curve of LDH/DNA was obtained with λ = 0.086. This parameter is considered suitable for the comparison of the effects of different oestrogens. Administration of Oe2 for 8 days beginning on the day of ovariectomy gave no linear dose-response curve of LDH/DNA. Administration of EOe caused a very marked increase of the specific activity of pyruvate kinase, LDH, M-type LDH and some slight, but significant decreases in isocitrate dehydrogenase, glutamate dehydrogenase, acid phosphatase and alkaline phosphatase. The changes of β-glucuronidase were only slight. The content of DNA per wet weight of endometrium decreased after oestrogen treatment, the protein content remained reasonably constant. It is concluded that, after stimulation with oestrogen, the rat endometrium produces the energy needed for its own growth mainly via anaerobic glycolysis and that the Krebs cycle plays a relatively small role.
ISSN:0804-4643
0001-5598
1479-683X
DOI:10.1530/acta.0.0960382