Human placental estradiol 17.beta.-dehydrogenase: evidence for inverted substrate orientation ("wrong-way" binding) at the active site

Abstract
Human placental estradiol 17.beta.-dehydrogenase (EC 1.1.1.62) was affinity labeled with 17.alpha.-estradiol 17-(bromo[2-14C]acetate) (10 .mu.M) or 17.beta.-estradiol 17-(bromo[2-14C]acetate) (10 .mu.M). The steroid bromoacetates competitively inhibit the enzyme (against 17.beta.-estradiol) with Ki values of 90 .mu.M (17.alpha. bromoacetate) and 134 .mu.M (17.beta. bromoacetate). Inactivation of the enzyme followed pseudo-first-order kinetics with a t1/2 = 110 min (17.alpha. bromoacetate) and t1/2 = 220 min (17.beta. bromoacetate). Amino acid analysis of the affinity radioalkylated enzyme samples from the two bromoacetates revealed that N.pi.-(carboxy[14C]methyl)histidine was the modified amino acid labeled in each case. Digestion with trypsin produced peptides that were isolated by reverse-phase high-performance liquid chromatography and found to contain N.pi.-(carboxy[14C]methyl)histidine. Both the 17.alpha. bromoacetate and also the 17.beta. bromoacetate modified the same histidine in the peptide Phe-Tyr-Gln-Tyr-Leu-Ala-His(.pi.-CM)-Ser-Lys. Previously, the same histidine had been exclusively labeled by estrone 3-(bromoacetate) and shown not to be directly involved in catalytic hydrogen transfer at the D-ring of estradiol. Therefore, this histidine was presumed to proximate the A-ring of the bound steroid substrate. The present results suggest that the 17.alpha. bromoacetate and 17.beta. bromoacetate D-ring analogues of estradiol react with the same active site histidine residue as estrone 3-(bromoacetate), the A-ring analogue of estrone. Moreover, as each of the estradiol 17-(bromoacetates) undergoes the reversible binding step at the enzyme active site, its D-ring is in a reversed binding position relative to that of the natural substrate 17.beta.-estradiol as it undergoes catalytic hydrogen transfer at the same active site.

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