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.