The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition. Genetic Testing Information. 1 Reaction 2 Isozymes 3 Nomenclature 4 Inhibitors 5 Biosynthetic pathway 6 Clinical significance 7 See also 8 References 9 Further reading. a 3β-hydroxy-Δ 5 -steroid + NAD + ⇌ a 3-oxo-Δ 5 -steroid + NADH + H + Nomenclature Edit. 3β-HSD is potently inhibited by azastene, cyanoketone, epostane, and trilostane. [4] Medroxyprogesterone acetate and medrogestone are weak inhibitors of 3β-HSD which may substantially inhibit it at high dosages.
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The two siblings seem to be affected by 3β-HSD2 deficiency; nevertheless, the two novel variants are likely to cause variable expressivity of the disease. 3β-HSD is responsible for the conversion of pregnenolone to progesterone, 17β-hydroxypregnenolone to 17β-hydroxyprogesterone, dehydroepiandrosterone (DHEA) to androstenedione and androstenediol to testosterone. 3β-HSD is encoded by two closely related genes located on chromosome 1 (1p13.1), HSD3B2 and HSD3B1, coding for type II and I isozymes, respectively. Type I isozyme (HSD3B1) is mainly expressed in the placenta and peripheral tissues, and type II isozyme (HSD3B2) is mainly expressed in the adrenal gland and gonads [4,5].
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