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Biomedical subjects

C A Strott

Publications and source records attributed to C A Strott.

At least 73 records · Page 4Linked to original sources
PubMed1978

Stimulation of steroid synthesis by normal rat adrenocortical cells in response to antimicrotubular agents.

The role of cytoplasmic microtubules in the process of steroidogenesis was examined in enzyme-dispersed and mechanically dispersed adrenocortical cells obtained from adult male rats. These cells were maintained in culture for periods of 2 h to 2 days and tested with various antimicrotubular drugs as well as ACTH and N6,O2-dibutyryl adenosine 3',5'-monophosphoric acid [(Bu)2cAMP]. The drugs tested, viz. colchicine, vinblastine, and nocodazole, were found to stimulate steroid synthesis in a dose-dependent fashion; the maximal degree of stimulation was found to be the same as that obtained with either ACTH or (Bu)2cAMP. When a maximal concentration of an antimicrotubular drug was mixed with a maximal concentration of either (Bu)2cAMP or ACTH, no additive effect on steroidogenesis was observed. The mixture of maximal concentrations of two antimicrotubular drugs produced a steroidogenic response that was less than when either drug was used alone. However, when submaximal concentrations of two antimicrotubular drugs were mixed, a synergistic response was noted. These antimicrotubular drugs are known to interfere with microtubular function by binding to specific sites on the tubulin protomer and inhibiting normal polymerization. Lumicolchicine, the photoinactivated form of colchicine, does not bind to tubulin and did not stimulate steroid synthesis. These studies support the notion that microtubules can influence the process of steroidogenesis.

Adrenal Cortex↗
PubMed1977

A pregnenolone-binding protein in soluble fraction of guinea pig adrenal cortex.

A pregnenolone-binding component has been detected in the soluble fraction of the guinea pig adrenal cortex. Enzymatic degradation studies revealed that the binding component was a protein. The binding was destroyed at 60 degrees but was not inhibited by sulfhydryl reactants. Pregnenolone was bound optimally at pH 7 to 7.5 The equilibrium association constant at 0 degrees was 10(7) M-1. The pregnenolone-binding protein had an apparent molecular weight of 58,000, as determined by gel filtration. With the exception of pregnenolone sulfate, structurally similar steroids did not interfere with pregnenolone binding. No such binding activity was detected in the guinea pig liver and kidney. Serum contained pregnenolone-binding activity which was distinguishable from the adrenal cytosol factor by a variet of physicochemical means. The physiological importance of this finding remains to be determined.

Adrenal Cortex↗
PubMed1972

Site of stimulation of aldosterone biosynthesis by angiotensin and potassium.

Studies were undertaken to determine what part of the aldosterone biosynthetic pathway is stimulated by angiotensin and potassium. The availability of a method for isolating the early portion of the aldosterone pathway and a new method for measuring plasma deoxycorticosterone permitted the design of experiments to determine whether angiotensin and potassium stimulate the pathway before deoxycorticosterone. To eliminate ACTH-dependent steroid synthesis, the experiments were performed in subjects receiving constant dosage of dexamethasone. To minimize the intra-adrenal conversion of deoxycorticosterone to corticosterone, all subjects also received constant dosage of metyrapone. Plasma deoxycortisol was measured as an index of the activity of the zona fasciculata. In the absence of changes in plasma deoxycortisol, one may infer that changes in plasma deoxycorticosterone represent changes in function of zona glomerulosa, the site of aldosterone formation. Under these conditions, human subjects responded both to angiotensin and to potassium with significant increases in plasma deoxycorticosterone but without significant increases in plasma deoxycortisol. In contrast, small doses of ACTH given under similar conditions never induced increases in plasma deoxycorticosterone without simultaneously inducing large increases in plasma deoxycortisol. It is concluded that the aldosterone-stimulating effects of angiotensin and potassium are, at least in part, consequences of stimulation of the biosynthetic pathway at some point before the formation of deoxycorticosterone so as to increase the availability of aldosterone precursors.

17-Hydroxycorticosteroids↗