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18-Hydroxylase (aldosterone synthase) – mineralocorticoid synthesis; 21-Hydroxylase – corticosteroid synthesis; Cytochrome P450 (CYP1, 2, 3) – estrogen metabolism; Hydroxysteroid dehydrogenases (and ketosteroid reductases) 3α-Hydroxysteroid dehydrogenase – androgen, progestogen, and neurosteroid synthesis and metabolism
Aldosterone synthase, also called steroid 18-hydroxylase, corticosterone 18-monooxygenase or P450C18, is a steroid hydroxylase cytochrome P450 enzyme involved in the biosynthesis of the mineralocorticoid aldosterone and other steroids. The enzyme catalyzes sequential hydroxylations of the steroid angular methyl group at C18 after initial 11β ...
Aldosterone stimulates Na + and water reabsorption from the gut, salivary and sweat glands in exchange for K +. Aldosterone stimulates secretion of H + via the H+/ATPase in the intercalated cells of the cortical collecting tubules; Aldosterone upregulates expression of NCC in the distal convoluted tubule chronically and its activity acutely. [18]
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The outermost layer, the zona glomerulosa is the main site for the production of aldosterone, a mineralocorticoid. The synthesis and secretion of aldosterone are mainly regulated by the renin–angiotensin–aldosterone system. The zona glomerulosa cells express a specific enzyme aldosterone synthase (also known as CYP11B2).
English: *Enzymes, their cellular location, substrates and products in human steroidogenesis. Shown also is the major classes of steroid hormones: progestagens, mineralocorticoids, glucocorticoids, androgens and estrogens.
Steroid 21-hydroxylase is a protein that in humans is encoded by the CYP21A2 gene.The protein is an enzyme that hydroxylates steroids at the C21 position on the molecule. [10] [11] Naming conventions for enzymes are based on the substrate acted upon and the chemical process performed.
It also catalyzes hydroxylation of progesterone to 11-deoxycorticosterone (DOC) in the mineralocorticoid pathway on its way from pregnenolone to aldosterone. [ 162 ] Deficient activity of this enzyme reduces the efficiency of cortisol synthesis, with consequent hyperplasia of the adrenal cortex and elevation of ACTH levels.