Meeting Abstract
P2.190 Saturday, Jan. 5 Decline in Mitochondrial Respiration in Post-Ovariectomy Mice is Ameliorated by Beta-Estradiol FERNANDEZ, WL*; NATHAN, BP; MENZE, MA; Eastern Illinois University; Eastern Illinois University; Eastern Illinois University mmenze@eiu.edu
The female sex hormone estrogen has potent neuroprotective properties. Some of these effects may be due to direct modulation of mitochondrial functions. We hypothesized that beta-estradiol treatment will improve mitochondrial bioenergetics in ovariectomized mice. Mice (C57BL/6J, female, 4-10 months-old) were ovariectomized via bilateral incision and control animals underwent sham surgery (Sham). Ovariectomized mice were divided into two groups: One group received a subcutaneous injection of 17-beta-estradiol (E2) dissolved in corn oil (30 ng/g) 24 h prior to synaptosome isolation (estradiol group). The second group received corn oil alone (OviX). Synaptosomes were isolated from the forebrain by Percoll gradient centrifugation. Oxygen consumption of permeabilized synaptosomes was measured using Clark-type polarographic electrodes at 37 ° C. State 4 respiration rates were determined in presence of 5 mM pyruvate, 2 mM malate, 10 mM glutamate, 10 mM succinate, and 2 mM ADP. Our results revealed that state 4 rates dropped significantly in OviX mice (5.55 ± 0.32 pmol O2•s-1• µ g -1 protein; n = 14, ±SE) compared to Sham (7.00 ± 0.28 pmol O2•s-1• µ g-1 protein; n = 8, ±SE, p < 0.05). Respiration rates after estrogen treatment (6.96 ± 0.53 pmol O 2•s-1• µ g-1 protein) were significantly increased compared to OviX (n = 6, ±SE; p < 0.05) and indistinguishable from Sham (p > 0.05). However, no differences in state 4 rates were observed among groups in absence of succinate. Our data suggest that estrogen directly impacts mitochondrial activity. Additional studies are being carried out to determine whether succinate dehydrogenase levels are altered by E2 administration.
