摘要:

Sonicates of human cultured lymphocytes metabolize (benzo(a)pyrene to at least two intermediates that bind covalently to deproteinized DNA in vitro. The major peak represents the 4,5-oxide bound to nucleoside(s). No correlation is found between ‘aryl hydrocarbon hydroxylase activity’ (or its inducibility) and benzo(a)pyrene metabolites generated by human lymphocytes and bound to DNA in vitro. Human liver microsomes produce in vitro at least six such reactive intermediates which, bound to deproteinized DNA nucleosides, are separable by chromatography. The major peak represents the 7,8-diol-9,10-epoxides bound to nucleoside(s): this highly reactive intermediate is believed to be one of the ultimate carcinogenic forms of benzo(a)pyr

ISSN:0031-7012    

DOI:10.1159/000136862

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

Index of accommodation of 32 frog sciatic nerves was studied with exponentially rising currents. Ethanol was mixed with normal Ringer’s solution at the following concentrations: 42, 85, 171, and 513 mM. We found a significant increase in the accommodation index. The results were attributed to the sodium conductance change and to a drop in membrane potential elicited by ethanol. The loss of the breakdown in the nerve accommodation curve was interpreted as the ethanol acting mainly on the thinner nerve fibres rather than on the large fibre

ISSN:0031-7012    

DOI:10.1159/000136863

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

The effects of intraperitoneal pretreatment, 48 h beforehand, with zinc sulphate (22, 44 or 88 mg/kg) were studied on gastric ulceration, gastric secretion and changes in stomach wall mast cell counts induced after 4 h by reserpine (5 mg/kg) given intraperitoneally to intact (unoperated for pylorus occlusion) or pylorus-occluded rats. Zinc sulphate dose-dependently antagonised the gastric actions of reserpine by preventing ulceration in the ruminal and glandular segments of the stomach, reducing acid secretion, and inhibiting mast cell degranulation which occurred mainly in the glandular mucosal layer. The relationship between these findings and the action of zinc on gastric mast cells is discussed.

ISSN:0031-7012    

DOI:10.1159/000136864

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

The spin state of cytochrome P450 ferric iron in vivo and in vitro was examined in freshly prepared liver microsomes from rabbit, guinea pig, hamster, mouse, and rat by room-temperature difference spectrophotometry. The administration of compounds which induce certain forms of P450 (phenobarbital, β-naphthoflavone, or 3-mefhylcholanthrene) to each of these species produces consistent detectable changes in the spin state of P-450 iron in vivo. Simple liquids of known relatively ‘pure’ type I, reverse type I, or type II character (cyclohexane, butanol-1, and octylamine-1, respectively) produce detectable changes in the in vitro spin state of P450 iron. By the method of off-balance spectrophotometry (in which microsomal cytochrome b5 is made equal in both cuvettes), we show that these differences in spin state in vivo and in vitro vary among the five mammalian species and are altered by prior treatment in vivo with the inducers of P450 and by addition in vitro of such chemicals as cyclohexane, butanol-1, and octylamine-1. The magnitude of the peak-to-trough height in type I, reverse type I, and type II difference spectra (or whether any spectrum is detected) is shown to depend largely on the in vivo spin state of the P450 iron in freshly prepared microsomes at the start of the experiment. The presence of a 410-nm trough in the type II difference spectrum is shown to represent a ligand having reverse type I character in the sixth coordination site of in vivo low spin iron. Our data therefore indicate that the sixth ligand for in vivo low spin P-450 ferric iron is a hydroxyl group from an adjacent amino acid residue of the P-450 protein (or moiety of similar ligand field strength, such as a water molecule) rather than a stronger ligand such as one having lone pair electrons from an N

ISSN:0031-7012    

DOI:10.1159/000136865

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

The norepinephrine (NE)-induced accumulation of cyclic AMP in incubated tissue slices of mouse lung was inhibited by chlorpromazine (CPZ) and to a lesser extent by haloperidol. In particulate lung fractions both agents blocked dopamine-sensitive adenylate cyclase to a greater degree than the NE-responsive enzyme. Again CPZ was more potent than haloperidol. Acute injections (½–8 h) of the neuroleptics usually resulted in lower steady state levels of pulmonary cyclic AMP and cyclic GMP following rapid (0.5 sec) tissue inactivation by microwave irradiation. On a subchronic injection schedule, the in vivo levels of pulmonary cyclic AMP tended to increa

ISSN:0031-7012    

DOI:10.1159/000136866

出版商:S. Karger AG    

年代:1978

数据来源: Karger

摘要:

Serum from adjuvant arthritic rats inhibits the concanavalin A- (Con A) and lipopolysaccharide-induced stimulation of lymph node cells, leaving the basal and phytohemagglutinin-stimulated 3H-thymidine incorporation unaffected. Con A-stimulated 3H-thymidine uptake is also inhibited in rat spleen and peripheral blood lymphocytes and in dog peripheral blood lymphocytes. The intensity of the inhibitory activity in serum is positively correlated with the intensity of the secondary lesions of adjuvant arthritis. Inhibitory activity was not found in serum from rats bearing nystatin-induced inflammation. Serum fractionation studies indicated that the inhibitory activity cannot be attributed to low molecular weight α2-glycoproteins or to γ-globulins and α2-macroglobulins, but it is present in a fraction migrating with β-globulins. The inhibitory activity in arthritic rat serum is reduced by treatment with non-steroidal anti-inflammatory drugs, but is unaltered by D-penicillamine. It is suggested that this inhibitory activity is part of the systemic response to an immunologically mediated inflammat

ISSN:0031-7012    

DOI:10.1159/000136867

出版商:S. Karger AG    

年代:1978

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000136868

出版商:S. Karger AG    

年代:1978

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137105

出版商:S. Karger AG    

年代:1967

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137106

出版商:S. Karger AG    

年代:1967

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000137107

出版商:S. Karger AG    

年代:1967

数据来源: Karger