Where is 5 alpha reductase produced

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The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Sex Disorders. Drug: testosterone enanthate Drug: duastride. Large families with affected members have been found in several countries, including the Dominican Republic, Papua New Guinea, Turkey, and Egypt. Mutations in the SRD5A2 gene cause 5-alpha reductase deficiency. The SRD5A2 gene provides instructions for making an enzyme called steroid 5-alpha reductase 2.

This enzyme is involved in processing androgens, which are hormones that direct male sexual development. Specifically, the enzyme is responsible for a chemical reaction that converts the hormone testosterone to DHT. DHT is essential for the normal development of male sex characteristics before birth, particularly the formation of the external genitalia.

Mutations in the SRD5A2 gene prevent steroid 5-alpha reductase 2 from effectively converting testosterone to DHT in the developing reproductive tissues. These hormonal factors underlie the changes in sexual development seen in infants with 5-alpha reductase deficiency. During puberty, the testes produce more testosterone. Researchers believe that people with 5-alpha reductase deficiency develop secondary male sex characteristics in response to higher levels of this hormone. Some affected people also retain a small amount of 5-alpha reductase 2 activity, which may produce DHT and contribute to the development of secondary sex characteristics during puberty.

This condition is inherited in an autosomal recessive pattern , which means both copies of the SRD5A2 gene in each cell have a mutation. Most often, the parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they do not show signs and symptoms of the condition. The autosomal recessive genetic disorder of 5 alpha-reductase deficiency has clearly shown that the requirement for DHT formation varies with different tissues.

In this syndrome genetic males contain normal male internal structures including testes, but exhibit ambiguous or female external genitalia at birth; at puberty they undergo partial virilization which includes development of a male gender identity even if brought up as females.

Their development suggests that testosterone itself is able to stimulate psychosexual behaviour, development of the embryonic wolffian duct, muscle development, voice deepening, spermatogenesis, and axillary and pubic hair growth; DHT seems to be essential for prostate development and growth, the development of the external genitalia and male patterns of facial and body hair growth or male-pattern baldness.

How different hormones operate to regulate genes via the same receptor is currently unknown, but appears to involve cell-specific factors. Future trials should focus on blocking multiple steroidogenic enzymes at once, such as in men with biochemical failure after local therapy or men with CR-CaP.

Blocking several different steps in steroidogenesis simultaneously may not allow CaP cells time to adjust to loss of androgen stimulation.

This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Academic Editor: Colleen Nelson. Received 15 Jul Revised 11 Sep Accepted 27 Sep Published 25 Dec Abstract Despite the discovery of 5 alpha-reduction as an enzymatic step in steroid metabolism in , and the discovery that dihydrotestosterone is more potent than testosterone in , the significance of 5 alpha-reduced steroids in human diseases was not appreciated until the discovery of 5 alpha-reductase type 2 deficiency in Introduction Testosterone T is the most abundant androgen in serum.

Background Steroids are a special type of lipid. Table 1. Figure 1. Table 2. Comparison between finasteride and dutasteride referenced in text. No expression was detected in dermal papillae or in sebaceous glands Thigpen et al. There was no correlation between enzyme activity at pH 5.

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