Steroid hormone biosynthesis 2

Laws and Penalties:  Concerns over growing illegal AAS abuse by teenagers, and many of the just discussed long-term effects, led Congress in 1991 to place the whole AAS class of drugs into Schedule III of the Controlled Substances Act (CSA).  Under this legislation, AAS are defined as any drug or hormonal substance, chemically and pharmacologically related to T (other than estrogens, progestins, and corticosteroids) that promotes muscle growth.  The possession or sale of AAS without a valid prescription is illegal.  Since 1991, simple possession of illegally obtained AAS carry a maximum penalty of one year in prison and a minimum $1,000 fine if this is an individual’s first drug offense.  The maximum penalty for trafficking (selling or possessing enough to be suspected of selling) is five years in prison and a fine of $250,000 if this is the individual’s first felony drug offense.  If this is the second felony drug offense, the maximum period of imprisonment and the maximum fine both double.  While the above listed penalties are for federal offenses, individual states have also implemented fines and penalties for illegal use of AAS.  State executive offices have also recognized the seriousness of AAS abuse and other drugs of abuse in schools. For example, the State of Virginia enacted a law that will allow student drug testing as a legitimate school drug prevention program (48, 49).

Human Growth Hormone is an injectable hormone that can be administered subcutaneously or intramuscularly. When injected subcutaneously, HGH carries a bioavailability of approximately seventy-five percent. When injected intramuscularly, HGH carries a bioavailability of approximately sixty-three percent. The mode of administration will also affect the half-life of the Somatropin hormone. When injected subcutaneously, it will carry a half-life of approximately hours. When injected intramuscularly, it will carry a half-life of approximately hours. While this is a rather short half-life regardless of the mode of administration, keep in mind the total effects far outlast these numbers due to the pronounced and significant increases in IGF-1 production that stretch far past the twenty-four hour mark.

We have also noted that 24-hour urinary estrogens can be a sensitive monitor of liver detoxification capability. Elevated urinary estrogens in normally-cycling women may indicate a history of exposure to liver stresses such as excessive environmental organic chemicals. Interventions intended to improve liver function result in a gradual normalization of the abnormal estrogen levels. Thus, measurement of urinary estrogens can give insight into other aspects of physiology. This phenomenon is also noted in peri- or post-menopausal women who have previously taken Premarin, and have switched to triple-estrogen replacement with less-than-optimal symptom relief.

FIGURE 2. Major Pathways of Steroid Biosynthesis.
The pathways outlined here are common to the adrenals, the gonads and, to some extent, to the fetoplacental unit. The first committed step is the conversion of cholesterol to pregnenolone, catalysed by the P-450scc enzyme, which is under pituitary hormone control (ACTH or LH depending on the tissue). Cholesterol side-chain removal is blocked specifically by aminoglutethimide , a steroid biosynthesis inhibitor. From pregnenolone, steroid biosynthesis can proceed either through the so-called "delta-5" pathway (17α-hydroxypregnenolone, dehydroepiandrosterone, testosterone), or through the "delta-4" pathway (progesterone onwards). Progesterone is the starting point for mineralocorticoid synthesis, whereas glucocorticoids are derived from its metabolite, 17α-hydroxyprogesterone. Estrogens are formed from androgens (androstenedione and/or testosterone). Most reactions are irreversible (as denoted by a single arrow). Reversible reactions (double arrows) depend on cofactor availability (. the NADP/NADPH ratio). [Abbreviations used here for the various enzymes are listed in the figure].

Sex hormone-binding globulin (SHBG) is thought to mainly function as a transporter and reservoir for the estradiol and testosterone sex hormones. However it has also been demonstrated that SHBG can bind to a cell surface receptor (SHBG-R). The SHBG-R has not been completely characterized. A subset of steroids are able to bind to the SHBG/SHBG-R complex resulting in an activation of adenylyl cyclase and synthesis of the cAMP second messenger. [19] Hence the SHBG/SHBG-R complex appears to act as a transmembrane steroid receptor that is capable of transmitting signals to the interior of cells.

Steroid hormone biosynthesis 2

steroid hormone biosynthesis 2

FIGURE 2. Major Pathways of Steroid Biosynthesis.
The pathways outlined here are common to the adrenals, the gonads and, to some extent, to the fetoplacental unit. The first committed step is the conversion of cholesterol to pregnenolone, catalysed by the P-450scc enzyme, which is under pituitary hormone control (ACTH or LH depending on the tissue). Cholesterol side-chain removal is blocked specifically by aminoglutethimide , a steroid biosynthesis inhibitor. From pregnenolone, steroid biosynthesis can proceed either through the so-called "delta-5" pathway (17α-hydroxypregnenolone, dehydroepiandrosterone, testosterone), or through the "delta-4" pathway (progesterone onwards). Progesterone is the starting point for mineralocorticoid synthesis, whereas glucocorticoids are derived from its metabolite, 17α-hydroxyprogesterone. Estrogens are formed from androgens (androstenedione and/or testosterone). Most reactions are irreversible (as denoted by a single arrow). Reversible reactions (double arrows) depend on cofactor availability (. the NADP/NADPH ratio). [Abbreviations used here for the various enzymes are listed in the figure].

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