Inhibition of mitochondrial Na-dependent Ca2+ efflux from rat brain stem by 17β-estradiol
Author(s) -
Snježana Petrović,
Maja Milošević,
Ivana Stanojević,
Nataša Veličković,
Dunja Drakulić,
Anica Horvat
Publication year - 2009
Publication title -
archives of biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.217
H-Index - 25
eISSN - 1821-4339
pISSN - 0354-4664
DOI - 10.2298/abs0902171p
Subject(s) - efflux , calcium , mitochondrion , homeostasis , chemistry , medicine , endocrinology , flux (metallurgy) , free nerve ending , calcium metabolism , membrane potential , microbiology and biotechnology , biophysics , biology , biochemistry , organic chemistry
The role of membrane-bound estradiol in modulation of mitochondrial Ca2+ flux in nerve endings isolated from rat brain stem was examined. Physiological concentrations of 17β-estradiol bind specifically to isolated mitochondria (Bmax 33.8 ± 2.5 fmoles estradiol/mg of protein, Km 0.185 ± 0.006 nmoles/l free estradiol). At concentrations ranging from 1 x 10-10 to 2 x 10-9 moles/l, estradiol significantly (by 23-28%) decreases mitochondrial Na-dependent calcium efflux. Decreased calcium efflux was associated with increased affinity of the Na+/Ca2+ exchanger for Na+ and decreased capacity of the exchanger to extrude Ca2+. Calcium ion efflux modulation and mitochondrial ion retention may be the way that 17β-estradiol exerts its role in nerve cell homeostasis
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