Estrogen conjugation, pathways

By increasing the activity of the kynurenine pathway, estrogens could also increase the requirements for PLP and make less available to act as the coenzyme for 5-hydroxytryptophan decarboxylase, or estrogen conjugates could displace PLP from the decarboxylase coenzyme directly. Even though in nonhuman mammals tryptophan hydroxylase, not the decarboxylase, is thought to be rate-limiting in serotonin synthesis (Jl), levels of decarboxylase are said to be so low in human brain... 

The principal pathways of transfer of andn>gen and estrogen conjugates... 

Approximately 50% of a dose of mestranol is de-methylated to form ethinyl estradiol. Ethinyl estradiol also can be deethinylated. Subsequently, the metabolism of these two synthetic estrogens proceeds by means of the same pathways as the natural steroid hormones. The principal metabolites of mestranol and ethinyl estradiol are hydroxylated derivatives that are conjugated with either glucuronic acid or sulfate. The synthetic steroid estrogens, in contrast to the natural estrogens, are excreted primarily in the feces. 

Because of the wide chemical diversity of estrogenic pharmaceutics, it is difficult to categorize the pathways for metabolic conversion and excretion. However, the majority of these reactions occur in the liver where they are inactivated by various hydro-xylation and oxidation reactions, although the major pathways involve conjugation and excretion in the urine and feces as sulfates and glucuronates. 

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