cholic acid is defective in people with cerebrovascular cholesterosis (CTX) and excretion of 5β-cholestane-3α, 7α, 12α, 25-tetrol connected, an intermediate product in the 25-hydroxylation pathway of cholic acid in the CTX. To set the enzymatic defect in CTX, two putative precursor colic, namely 5β- [7β-3H] cholestane-3α, 7α, 12α-triol and 5β- [24-14C] cholestane-3a, 7a, 12α, 24S, 25 -Pentol were examined both in vivo and in vitro experiments. A third precursor 5β- [7β-3H] cholestane-3α, 7α, 12α, 25-tetrol was compared with them in vitro.
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