Subcellular action of estradiol-17 beta in a freshwater prawn Macrobrachium rosenbergii.
Injections with different doses (0.1, 0.25, 0.5, 1.0, 2.0, and 4.0 micrograms/g) of estradiol-17 beta (E2), administered three days consecutively, showed a statistically significant increase in mitochondrial Na(+)-K(+)-ATPase, cytosolic malate dehydrogenase, and cytosolic glucose-6-phosphate dehydrogenase activities in a dose-dependent manner in the hepatopancreas of the freshwater prawn (Macrobrachium rosenbergii) on the 4th day of treatment compared to the control values. A lower dose of 0.05 microgram/g was without any effect on these enzyme activities. A uniform increase in the Mg(2+)-ATPase activity was observed after injections with 0.5, 1.0, and 2.0 micrograms/g of E2. Ergosterol, a nonsex steroid did not show any change in the malate dehydrogenase and glucose-6-phosphate dehydrogenase activities on which this compound was tested at a 2.0 micrograms/g dose, compared to the control values. Simultaneous injection of tamoxifen (0.5 microgram/g), an antiestrogenic compound, with E2 (2 micrograms/g) caused inhibition of the E2-induced rise in mitochondrial Na(+)-K(+)-ATPase and cytosolic NADP-linked malate dehydrogenase activities. Conversely, tamoxifen (0.5 and 1.0 microgram/g) behaved as an estrogen agonist to the response (increase) of Mg(2+)-ATPase and cytosolic glucose-6-phosphate dehydrogenase activities. Potentiation of the estrogen effect with tamoxifen (1.0 microgram/g) was observed in these enzyme activities when used simultaneously with E2 (2 micrograms/g). Use of cycloheximide (0.5 mg/liter), a protein synthesis blocker, inhibited the inhibited the E2 (2 micrograms/g)-induced increase in all the enzyme activities studied. The data show specific and prominent subcellular action of estrogen with an indication of its role in energy-dependent ion transport and metabolic activation in hepatopancreas of the freshwater prawn.
Ghosh
D
D
Department of Animal Physiology, Bose Institute, Calcutta, India.
Ray
A K
AK
D000818:Animals; D017301:Ca(2+) Mg(2+)-ATPase / Q000032:analysis / Q000378:metabolism; D003513:Cycloheximide / Q000494:pharmacology; D003600:Cytosol / Q000201:enzymology*; D004305:Dose-Response Relationship, Drug; D004527:Egg Proteins; D015387:Egg Proteins, Dietary / Q000378:metabolism; D004790:Enzyme Induction; D004958:Estradiol / Q000008:administration & dosage / Q000494:pharmacology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000032:analysis / Q000378:metabolism; D006801:Humans; D007267:Injections; D008099:Liver / Q000201:enzymology / Q000648:ultrastructure; D008291:Malate Dehydrogenase / Q000032:analysis / Q000378:metabolism; D008297:Male; D008928:Mitochondria / Q000201:enzymology*; D033541:Palaemonidae / Q000201:enzymology*; D010179:Pancreas / Q000201:enzymology / Q000648:ultrastructure; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis / Q000378:metabolism; D013629:Tamoxifen / Q000494:pharmacology
D004527:Egg Proteins; D015387:Egg Proteins, Dietary; D004965:Estrogen Antagonists; D013629:Tamoxifen; D004958:Estradiol; C001549:lipovitellin; D003513:Cycloheximide; D008291:Malate Dehydrogenase; C031917:malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+); D005954:Glucosephosphate Dehydrogenase; D017301:Ca(2+) Mg(2+)-ATPase; D000254:Sodium-Potassium-Exchanging ATPase