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The properties of estrone (E1) and dehydroepiandrosterone (DHEA) sulfatase activities are reported. Endometrial biopsy specimens were obtained using a Novak curette. Cycle stage was assessed from histological dating of endometrium, plasma estradiol and progesterone levels, and patient history. Both sulfatases are membrane-bound enzymes. The optimum pHs in Tris-HCl buffer were 6.5 for E1 sulfatase and 7.3 for DHEA sulfatase. Lowest activities and different optimum pHs were obtained with imidazole, maleate, or acetate buffers. DHEA sulfatase is more sensitive to thermal inactivation than E1 sulfatase. From kinetic studies, apparent Km values of 3.1 microM for E1 sulfatase and 5.7 microM for DHEA sulfatase were calculated. Noncompetitive inhibition of E1 sulfatase by DHEA sulfate and of DHEA sulfatase by E1 sulfate were demonstrated. The effects of inorganic ions and unconjugated steroids were also tested. These results are consistent with two different activities hydrolyzing E1 or DHEA sulfates. Neither activity varies during normal menstrual cycles nor is not correlated to plasma progesterone or 17 beta-estradiol levels. An isolated increase in E1 sulfatase occurred in the proliferative phase of irregular menstrual cycles, postantibiotic-treated salpingitis, or hyperplastic endometrium.

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We report the results of an ultrastructural study of the hyperkeratotic epidermis in 23 cases of palmoplantar keratoderma (PPK) comprising 8 inherited keratoderma, 8 keratoderma climactericum in menopausal women and 7 symptomatic keratoderma. In all but one of the cases of inherited PPK and keratoderma climactericum, composite keratohyalin (KH) granules were found in granular cells of the interductal epidermis, which were similar to those found in the rat and in some other conditions. In the cases of symptomatic keratoderma, e.g. secondary to eczema, the appearance of the KH granules did not differ from that of granules observed in two normal plantar skin samples. While the real role played by these granules is unknown, they could constitute a differentiation marker of intraepidermal duct cells, and their abundance in PPK suggest that intraepidermal sweat ducts may play a part in PPK histogenesis.

We investigated the activity of estrone sulfatase in normal and pathological endometrium. In normal endometrium, the estrone sulfatase activity [pmol E1 X min-1 X (mg prot)-1] was 23.13 +/- 8.44 (mean +/- SD). An increase (p less than 0.01) of estrone sulfatase activity (62.81 +/- 21.97) was noted in mild endometrial hyperplasia. In focal hyperplasia (when the measurements were performed in the normal endometrial biopsies) such an increase was not noted (19.10 +/- 5.33). Estrone sulfatase activities of moderate hyperplasia (25.30 +/- 11.40) and endometrial neoplasia (30.30 +/- 9.57) were in the same range as in normal endometrium. Treatment with progestagen simultaneously reduced hyperplasia and estrone sulfatase activity. But when morphologically abnormal endometrium persisted after treatment, estrone sulfatase activity remained increased. The increase of estrone sulfatase activity appeared to be specific to mild endometrial hyperplasia. The role of estrone sulfatase in the pathogenesis of endometrial hyperplasia is discussed.