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The effects of the alpha 1-adrenergic agonist methoxamine and the alpha 2-adrenergic agonist clonidine on isoproterenol stimulated adenylate cyclase activity were examined in plasma membranes prepared from female human subcutaneous adipose tissue. It was found that in the presence of 10 microM GTP and 100 mM NaCl increasing concentrations of both agonists inhibited basal and isoproterenol-stimulated adenylate cyclase activity. The inhibitory action of 5 x 10(-7) M clonidine could not be overcome by increasing concentrations of isoproterenol. These results suggest both alpha 1- and alpha 2-adrenergic agonists inhibit beta-agonist-stimulated adenylate cyclase activity in human adipose tissue.

Aromatase cytochrome P-450 (P-450AROM) was partially purified from human placental microsomes by hydrophobic affinity chromatography using Phenyl-Sepharose and ion-exchange chromatography on DEAE-cellulose. The resulting preparation had a specific activity of 2 nmol/mg protein with respect to cytochrome P-450 content and displayed a type I difference spectrum upon addition of the substrate androstenedione. When the cytochrome P-450-enriched fractions were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis and stained with Coomassie blue, there was an enrichment of two proteins having apparent molecular weights of 50,000 and 55,000. The bands containing these proteins were removed from unstained polyacrylamide gels and injected separately or together into three rabbits. An aliquot of the serum or an immunoglobulin (IgG) fraction prepared from the serum of the rabbit injected with the 55-kDa band or with both the 50- and 55-kDa bands inhibited aromatase activity of human placental microsomes by 80%; this IgG had no effect on 17 alpha-hydroxylase or 21-hydroxylase activities of human fetal adrenal microsomes. In contrast, the serum of the rabbit injected with the 50-kDa band had little capacity to inhibit placental aromatase activity. By immunoblot analysis, it was found that the IgG from the serum of the rabbit immunized with the 55-kDa protein bound specifically to a protein of 55 kDa in human placental microsomes. Monoclonal antibodies were prepared from a hybridoma cell line derived from the spleen cells of mice immunized against the 55-kDa protein. The monoclonal IgG was covalently linked to a Sepharose 4B column and was used for immunoaffinity chromatography of cytochrome P-450AROM. The finding that cytochrome P-450 and the 55-kDa protein were selectively retained by the affinity column and eluted with NaCl (2 M) and glycine (0.2 M, pH 3.0) and that this fraction contained aromatase activity upon reconstitution with purified NADPH-cytochrome P-450 reductase and phospholipid, is indicative that the 55-kDa protein is indeed cytochrome P-450AROM. These findings are also indicative that both the monoclonal and polyclonal IgGs are specific for human cytochrome P-450AROM.

As more people learn about prenatal diagnosis, medical personnel are increasingly being asked to perform these procedures in both low-risk pregnancies and for purposes of sex selection. Analysis of present legal rules illustrates that it is highly unlikely genetic counselors will be subjected to legal liability for refusing to provide prenatal diagnosis in these situations. This freedom from liability will probably continue into the foreseeable future, despite recent developments in the areas of informed consent and allocation of scarce medical resources that tend to limit the traditionally broad deference given to medical personnel.

Male lycosid spiders were prevented from using one palp during the first third of copulation by a sling that we then cut to free the palp. Initial insertion durations of the treated palp were significantly shorter than those shown concurrently by the much-used normal palp; they showed temporal patterning unaffected by use of the normal palp. Data indicate that there are relatively independent control mechanisms for each palp and support the hypothesis that fatigue causes the increased duration of successive palpal insertions. Our data also suggest that normal matings terminate due to maximal use of either palp by the male.

Whether peptide hormones other than ACTH may be responsible for the difference in size or rate and pattern of steroidogenesis of the fetal zone (FZ) compared to those of the neocortex (NC) of the human fetal adrenal gland is controversial. In the present investigation, the activity of adenylate cyclase in membrane fractions of separated zones of the human fetal adrenal gland was determined. Basal adenylate cyclase activity was 2- to 3-fold greater in NC than in FZ membrane fractions. The addition of ACTH-(1-24) stimulated adenylate cyclase activity in both zones, but the activity was more sensitive to ACTH (10(-10) M) in NC fractions than in FZ fractions (10(-7) M). In addition to ACTH-(1-24), the effect of other ACTH-related peptides on the activity of adenylate cyclase in the separated zones of the adrenal gland was investigated. 16K fragments 2-36, gamma 3MSH, alpha MSH, beta-endorphin, leu-enkephalin, and met-enkephalin, as well as hCG, FSH, prostaglandin E2, prostaglandin F2 alpha, epinephrine, and norepinephrine did not stimulate adenylate cyclase activity in either zone. It is concluded that basal and ACTH-(1-24)-stimulated adenylate cyclase activities are greater in NC than in FZ membrane fractions. In addition, the results of the present investigation do not support the concept that other ACTH-related peptides or peptide or protein hormones increase steroidogenesis by stimulating adenylate cyclase activity in the human fetal adrenal gland.

Prior studies indicate that the monoamine oxidase inhibitors (MAOI) harmine and iproniazide inhibit N-acetyltransferase activity from liver. In this report we have demonstrated that harmine and harmaline are potent inhibitors of N-acetyltransferase, purified from hamster and rat liver. However, other MAOI such as deprenyl, clorgyline, methysergide, cyproheptadine, phenelzine, pargyline, methyltryptamine and tranylcypromine have either no effect, or only trivial effects on N-acetyltransferase. There is no correlation between a compound's properties as an MAO and N-acetyltransferase inhibitor. One must consider the inhibitory effect of harmine and harmaline on both MAO and N-acetyltransferase when evaluating the effects of these compounds on physiological processes.