Detail of "9025-82-5"

Reference

Inhibition by cortisol of human natural killer (NK) cell activity

Inhibition by cortisol of human natural killer (NK) cell activity. Gatti, Giovanni; Cavallo, Rossana; Sartori, Maria Luisa; Del Ponte, Daniela; Masera, Rosa; Salvadori, Alessandro; Carignola, Renato; Angeli, Alberto (Dip. Biomed., Univ. Torino, Turin 10133, Italy). J. Steroid Biochem., 26(1), 49-58 (English) 1987. CODEN: JSTBBK. ISSN: 0022-4731. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 15 Preincubation for 20 h of human peripheral blood mononuclear (PBM) cells drawn from healthy donors with 1 ′ 10-8-1 ′ 10-5 M cortisol [50-23-7] decreased natural killer cell (NKC) cell activity.In this article, certain chemicals are used. Some of their cas registry numbers are 152-58-9 and 50-23-7 The magnitude of the suppression was directly related to the steroid concn. and inversely related to the no. of effector cells. Cortisol minimized the enhancement of NK cytotoxicity obtainable in the presence of immune interferon (IFN-g). A higher suppression was achieved after sequential exposure of PBM cells to cortisol and equimolar levels of PGE2 [363-24-6]. The concomitant incubation with theophylline and IBMX failed to enhance the cortisol-induced suppression, whereas PGE2-dependent inhibition increased after exposure of PBM cells to methylxanthines. The inhibitory effect of cortisol was partially or totally prevented by the concomitant incubation with equimolar amts. of 11-deoxycortisol [152-58-9] and RU 486 [84371-65-3], but not of progesterone. Treatment of NK effectors with a monoclonal anti-human corticosteroid-binding globulin (CBG) antibody enhanced the spontaneous NK activity and partial suppressed cortisol-mediated effects. Evidently, endogenous glucocorticoids play a role in regulation of NK cell-mediated cytotoxicity. Since the effect of cortisol was additive to that of PGE2 and was not changed by phosphodiesterase [9025-82-5] inhibitors, the hormone acts at a level different from the adenylate cyclase [9012-42-4]-phosphodiesterase system. Data obtained with the use of antiglucocorticoids and the anti-CBG antibody are compatible with a role both of high-affinity glucocorticoid receptors and of CBG in mediating cortisol action on the human NK cell activity. .

Biochemical and ultrastructural investigation of the effect of Stelazine (trifluoperazine) on Hymenolepis diminuta (Cestoda)

Biochemical and ultrastructural investigation of the effect of Stelazine (trifluoperazine) on Hymenolepis diminuta (Cestoda). Hipkiss, Jayne B.; Skinner, A.; White, C. J. Branford (Dep. Biol., Oxford Polytech., Headington/Oxford OX3 0BP, UK). Parasitology, 94(1), 135-49 (English) 1987. CODEN: PARAAE. ISSN: 0031-1820. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 12 The effects of the phenothiazine, Stelazine [440-17-5], on H. diminuta were investigated. 92-84-2 and 9000-83-3 which are cas registry numbers are also used here. The cestode was incubated for 10 min at 37° with 1 mM trifluoperazine, in the presence and absence of Ca2+. Assay of brush border enzymes showed that drug treatment lowered the activities of alk. phosphatase [9001-78-9], Ca2+ ATPase [9000-83-3], 5'-nucleotidase [9027-73-0], and type 1 phosphodiesterase [9025-82-5]. This occurred in parallel with a significant redn. in tegumental protein. Under these conditions gross changes in ultrastructural appearance and cellular organization were obsd. There was a lack of ordered microtriches and the distal cytoplasm was absent. Glycogen granules were scattered throughout the cytoplasm within the subtegumental layer. The connective tissue also appeared to be in some disarray. The effects of Stelazine appeared to be dependent on time and were increased when Ca2+ was included in the incubation medium. Incubation with the less hydrophobic phenothiazine trifluoperazine sulfoxide [1549-88-8] had minimal effect on the integrity of the cestode. Apparently, certain phenothiazines may be considered as potential cestocidal agents. .