Steroidogenic enzymes

In humans, the CYP17A1 gene is largely associated with endocrine effects and steroid hormone metabolism. [21] [22] [23] Furthermore, mutations in the CYP17A1 gene are associated with rare forms of congenital adrenal hyperplasia, in particular 17α-hydroxylase deficiency/17,20-lyase deficiency and isolated 17,20-lyase deficiency. Overall, CYP17A1 is an important target for inhibition in the treatment of prostate cancer because it produces androgen that is required for tumor cell growth. [24] [25] Currently, the FDA has approved only one CYP17A1 inhibitor, abiraterone, which contains a steroidal scaffold that is similar to the endogenous CYP17A1 substrates. Abiraterone is structurally similar to the substrates of other cytochrome P450 enzymes involved in steroidogenesis, and interference can pose a liability in terms of side effects. Using nonsteroidal scaffolds is expected to enable the design of compounds that interact more selectively with CYP17A1. [25] Potent inhibitors of the CYP17A1 enzyme provide a last line defense against ectopic androgenesis in advanced prostate cancer. [26]

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Biosynthesis of steroid hormones requires a battery of oxidative enzymes located in both mitochondria and endoplasmic reticulum. The rate-limiting step in this process is the transport of free cholesterol from the cytoplasm into mitochondria. Within mitochondria, cholesterol is converted to pregnenolone by an enzyme in the inner membrane called CYP11A1. Pregnenolone itself is not a hormone, but is the immediate precursor for the synthesis of all of the steroid hormones. The following table delineates the enzymes required to synthesize the major classes of steroid hormones.

One study has been conducted in athletes given D-aspartic acid supplementation at a dose of 3g daily for 28 days, and there was a failure to increase testosterone concentrations when measured at 28 days. [32] This study noted a statistically significant induction of serum D-aspartate oxidase (DAO) which degrades D-aspartate [53] to a near doubling; [32] this suggests a possible form of negative feedback, and aromatase (may also be induced by D-aspartic acid [24] ) was not thought to contribute due to estrogen being unchanged.

Steroidogenic enzymes

steroidogenic enzymes

One study has been conducted in athletes given D-aspartic acid supplementation at a dose of 3g daily for 28 days, and there was a failure to increase testosterone concentrations when measured at 28 days. [32] This study noted a statistically significant induction of serum D-aspartate oxidase (DAO) which degrades D-aspartate [53] to a near doubling; [32] this suggests a possible form of negative feedback, and aromatase (may also be induced by D-aspartic acid [24] ) was not thought to contribute due to estrogen being unchanged.

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