Steroid 11β-hydroxylation in beef adrenal cortex mitochondria. Binding affinity and capacity for specific [<sup>14</sup>C]-labeled steroids and for tritium-labeled metyrapol, an inhibitor of the 11β-hydroxylation reaction

Satre, Michel; Vignais, Pierre V.

doi:10.1021/bi00707a029

Cited by 32 publications

(18 citation statements)

References 45 publications

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“…Willmer's suggestion that steroid hormones interdigitate with, and alter the permeability of, lipids in the plasma membrane, lost currency as evidence that steroids bind to intracellular proteins (nuclear receptors) and stimulate protein synthesis began to accumulate from 1961 onwards [65,66]. However, in 1974 Satre and Vignais described corticosterone binding to mitochondrial preparations from the adrenal and kidney [67], a finding that eventually extended to other cell types [68]. A series of authors provided evidence for membrane-bound steroid recognition sites in the brain [69-71]; among these, Towle and Sze demonstrated specific corticosterone binding to plasma membrane preparations from rat brain synapses [72].…”

Section: Putative Membrane Receptors - Pirates With Legs To Stand On?mentioning

confidence: 99%

Corticosteroids: way upstream

et al. 2010

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Studies into the mechanisms of corticosteroid action continue to be a rich bed of research, spanning the fields of neuroscience and endocrinology through to immunology and metabolism. However, the vast literature generated, in particular with respect to corticosteroid actions in the brain, tends to be contentious, with some aspects suffering from loose definitions, poorly-defined models, and appropriate dissection kits. Here, rather than presenting a comprehensive review of the subject, we aim to present a critique of key concepts that have emerged over the years so as to stimulate new thoughts in the field by identifying apparent shortcomings. This article will draw on experience and knowledge derived from studies of the neural actions of other steroid hormones, in particular estrogens, not only because there are many parallels but also because 'learning from differences' can be a fruitful approach. The core purpose of this review is to consider the mechanisms through which corticosteroids might act rapidly to alter neural signaling.

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Section: Putative Membrane Receptors - Pirates With Legs To Stand On?mentioning

confidence: 99%

Corticosteroids: way upstream

et al. 2010

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“…Estradiol has been reported to bind to a specific protein in rat pancreatic acinar cells which is localized in the rough endoplasmatic reticulum and mitochondria [30]. Specific binding sites have also been found for deoxycorticosterone, deoxycortisol, corticosterone, and progesterone in beef adrenal cortex mitochondria [31], and for corticosterone in rat liver mitochondria [32]. To our knowledge, there is no evidence of estradiol binding to mitochondria isolated from synaptosomes.…”

mentioning

confidence: 99%

Binding of estradiol to synaptosomal mitochondria: physiological significance

Horvat¹,

Nikezić²,

Petrović³

et al. 2001

CMLS, Cell. Mol. Life Sci.

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The subsynaptosomal distribution and specific binding of 17beta-estradiol in vitro to mitochondria isolated from presynaptic nerve endings of female rat brain were examined. 17Beta-estradiol is (i) distributed unequally in synaptosomes and mitochondria posses the highest capacity to bind estradiol with respect to the available amount of the hormone. (ii) Estradiol binds specifically to isolated synaptosomal mitochondria. A Michaelis-Menten plot of specific binding was sigmoidal within a concentration range of 0.1-5 nM of added estradiol, with a saturation plateau at 3 nM. Binding of higher estradiol concentrations demonstrated an exponential Michaelis-Menten plot, indicating non-specific binding to mitochondria. Vmax and Km for the sigmoidal-shape range were estimated as 46 +/- 6 fmol of estradiol/mg of mitochondrial proteins and 0.46 +/- 0.07 nM free estradiol respectively. (iii) Estradiol binding is not affected by the removal of ovaries. The results show that inhibition of Na-dependent Ca2+ efflux from mitochondria by estradiol occurs according to an affinity change of the translocator for Na+, at the same estradiol concentrations that show specific binding to mitochondrial membranes. These data imply that physiological concentrations of estradiol, acting on mitochondrial membrane properties, extragenomically modulate the mitochondrial, and consequently the synaptosomal content of Ca2+, and in that way exert a significant change in nerve cell homeostasis.

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“…The present results indicate that glutethemide, an inhibitor of cholesterol 20tr-hydroxylase (Kahnt and Neher, 1966), metyrapone, an inhibitor of cytochrome P-450-linked reactions (Satre and Vignais, 1974) and spirocyanoketone, an inhibitor of C19-and C2,-3P-hydroxysteroid dehydrogenase (Goldman and Sheth, 1973) can inhibit the stimulatory effect of cGTH on androgen production by carp testis. The fact that the stimulatory effect of cGTH can be almost completely abolished by glutethemide indicates that the conversion of cholesterol to pregnenolone is necessary for expression of cGTH effect on androgen synthesis.…”

Section: Discussionmentioning

confidence: 50%

The mode of action of carp gonadotropin on the stimulation of androgen production by carp testis in vitro

Chang

Huang

1982

General and Comparative Endocrinology

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Carp gonadotropin (cGTH) can stimulate carp testis to produce androgen in vitro. This action can be mimicked by dibutyryl CAMP (Bt, CAMP) and prostaglandins (PG). Btp CAMP can enhance the androgen production when submaximal doses of cGTH are used but cannot do so when maximal dose of cGTH is used. PG F,,is more effective than PG E, and E,. Both the inhibitors of RNA and protein synthesis can interfere the stimulatory effect of cGTH. Actinomycin D has 87% while cycloheximide has 100% inhibition. The stimulatory effect of cGTH is much more dependent on de nova protein synthesis than on RNA synthesis. In addition, steroidogenesis inhibitors, glutethemide, metyrapone, and spirocyanoketone, can also inhibit the stimulatory effect of cGTH on androgen production.

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Steroid 11β-hydroxylation in beef adrenal cortex mitochondria. Binding affinity and capacity for specific [¹⁴C]-labeled steroids and for tritium-labeled metyrapol, an inhibitor of the 11β-hydroxylation reaction

Cited by 32 publications

References 45 publications

Corticosteroids: way upstream

Corticosteroids: way upstream

Binding of estradiol to synaptosomal mitochondria: physiological significance

The mode of action of carp gonadotropin on the stimulation of androgen production by carp testis in vitro

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Steroid 11β-hydroxylation in beef adrenal cortex mitochondria. Binding affinity and capacity for specific [14C]-labeled steroids and for tritium-labeled metyrapol, an inhibitor of the 11β-hydroxylation reaction

Cited by 32 publications

References 45 publications

Corticosteroids: way upstream

Corticosteroids: way upstream

Binding of estradiol to synaptosomal mitochondria: physiological significance

The mode of action of carp gonadotropin on the stimulation of androgen production by carp testis in vitro

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Steroid 11β-hydroxylation in beef adrenal cortex mitochondria. Binding affinity and capacity for specific [¹⁴C]-labeled steroids and for tritium-labeled metyrapol, an inhibitor of the 11β-hydroxylation reaction