The effects of gonadal steroid hormone, 17 beta-estradiol (E-2), in vitro o
n rat brain mitochondria Ca2+ movement were investigated. Intrasynaptosomal
mitochondria Ca2+ uptake via an energy-driven Ca2+ uniporter have K-m = 11
2.73 +/- 7.3 mu mol.l(-1) and V-max = 21.97 +/- 1.7 nmol Ca-45(2+) mg(-1).
Ca2+ release trough a Na+/Ca2+ antiporter was measured with a K-m for Na+ o
f 43.7 +/- 2.6 mmol.l(-1), and V-max of 1.5 +/- 0.3 nmol Ca-45(2+) mg(-1).
Addition of estradiol in preincubation mixture did not affect the uptake of
Ca2+ mediated by the ruthenium red-sensitive uniporter, while it produced
biphasic effect on Na-dependent Ca2+ efflux. Estradiol at concentrations up
to 1 nmol.l(-1) decreased the efflux significantly (63% inhibition with re
spect to the control), and at concentrations above 10 nmol.l(-1) increased
it exponentially. The maximum inhibiting concentration of estradiol (0.5 nm
ol.l(-1)) increased the affinity of the uniporter (K-m reduced by about 30%
), without affecting significantly the capacity (V-max) for Na+. The result
s presented suggest that estradiol inhibits Na-dependent Ca2+ efflux from m
itochondria and acts on mitochondrial retention of Ca2+, which may modulate
mitochondrial and consequently synaptosomal content of Ca2+, and in this w
ay exerts its role in the homeostasis of calcium in nerve terminals.