Effect of alkyl phosphates on beta-glucuronidase in rats: release of beta-glucuronidase from liver microsomes into serum.
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Biomedical subjects
Publications and source records attributed to Y Horiuchi.
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Acidic glycosaminolglycans (AGAG) in human plasma were studied by enzymatic and electrophoretic procedures after fractionation by gel filtration on Sephadex G-100. Galactosaminoglycans were the predominant acidic glycosaminoglycans in the small molecular weight fraction, but glucosaminoglycans were predominant in the macromolecular weight fraction. The major constituents of plasma AGAG were estimated as udersulfated chondroitin sulfate isomers followed by a lesser amount of hyaluronic acid characterized by susceptibility to specific chondroitinases and streptomyces hyaluronidase. In addition, the presence of small amounts of heparan sulfate and oversulfated chondroitin sulfate in human plasma was indicated.
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Human red cells sensitized with one of the Rh antisera (Ripley) form rosettes (Fc-rosette) with human B lymphocytes and the rosettes are well inhibited by aggregated human IgG. As synovial fluids from patients with rheumatoid arthritis are usually hypocomplementaemic and frequently contain immune complexes, they were used for the inhibition of Fc-rosette formations in this study. The Fc-rosette inhibitory rates were inversely correlated with the levels of CH50 and C4 in the synovial fluids. Fractionation studies of the synovial fluids by ultracentrifugation and Sephadex G200 gel filtration indicated that main inhibitory activities were present in macromolecular fractions. Reduction and alkylation of the synovial fluids resulted in marked reductions of inhibitory activities. The tested synovial fluids did not contain anti-HLA activity as assessed by the microcytotoxicity test. The Fc-rosette inhibitory rates were not correlated with the levels of C3 and immunoglobulins, nor with the activity of rheumatoid factors in the synovial fluids. These results indicate that the Fc-rosette formations are inhibited by the immune complexes contained in the synovial fluids and it was confirmed that the Fc-rosette inhibition test is a simple and sensitive method for the detection of circulating immune complexes.
Preferential enhancement of IgE antibody response was observed in BALF/c mice by the administration of Bordetella pertussis with antigen (DNP-Salmonella). Correlation between B cell mitogenic activity and adjuvant action among B. pertussis, Salmonella, lipopolysaccharide of Escherichia coli and Ficoll was examined but was not found. Thymus-derived cells seemed necessary to develop adjuvant action of B. pertussis since antibody response in athymic nude mice was not influenced by B. pertussis. Helper function of adoptively transfered spleen cells was enhanced by immunization of the donor mice with carrier antigen in the presence of B. pertussis. The magnitude of enhancement was greatest in IgE class. The results indicated that preferential enhancement of IgE antibody formation by B. pertussis is mediated by the augmentation of carrier-specific helper function.
Characterization and purification of the allergenic components of the house dust mite, Dermatophagoides farinae, were investigated. It was found that the mite antigen was heat-stable, pronase-sensitive, and periodate-resistant, which suggested that the antigenic determinants of the mite antigen resided mainly in the protein component. Purification of the mite antigen was tried using Sephadex G-150, DEAE cellulose, and isoelectrofocusing columns. The most potent allergenic fraction was around 20,000-30,000 in molecular weight, although the allergenic activity spread in a wide molecular weight range. Prausnitz-Küstner type skin reactions were performed on rats using mouse homocytotropic antibodies for allergenic evaluation, and the clinical usefulness of this method is discussed.
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Previous reports described that human red cells sensitized with one of Rh antisera (Ripley) make rosette formations (Fc-rosette with some lymphocytes. These Fc-rosettes were well inhibited by aggregated human IgG as well as hypocomplementemic systemic lupus erythematosus (SLE) sera and rheumatoid synovial fluids. In the present study, Fc-receptor bearing lymphocytes were considerably reduced in peripheral bloods of SLE (16.0 +/- 7.6%) and rheumatoid synovial fluids (15.6 +/- 5.3%). On the other hand, EAC-rosette formation rates of peripheral bloods of SLE (32.0 +/- 13.2%) and rheumatoid synovial fluids (30.3 +/- 11.2%) did not significantly differ from normal peripheral bloods (28.3 +/- 2.9%). E-rosette forming lymphocytes were reduced in peripheral bloods of SLE (48.7 +/- 15.7%) and in rheumatoid synovial fluids (49.0 +/- 14.6%) whereas 61.7 +/- 8.6% in normal peripheral bloods. Reduced Fc-rosette formation rates correlated well with the Fc-rosette inhibitory rates. In addition, eluates from the lymphocytes in rheumatoid synovial fluids also inhibited Fc-rosette formation. These results suggested that immune complexes present in peripheral bloods of SLE and rheumatoid synovial fluids are bound to the Fc-receptors on the lymphocytes, block the additional binding of the sensitized red cells, and result in the reduction of Fc-rosette formation.
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Purified or crude sera of several different phenotypes of alpha1-antitrypsin were treated with neuraminidase. The mobility of the alpha1-antitrypsin zone was delayed on starch gel electrophoresis following incubation. Treated, M-type alpha1-antitrypsin migrated in a manner similar to the untreated S type. Treated S migrated in a similar way to the untreated Z, and treated Z did so more slowly or cathodally. After exhaustive treatment, alpha1-acidglycoprotein bands appeared near the usual M or F positions. Treated samples still possessed the antigenic activity of alpha1-antitrypsin. The concentration and trypsin-inhibitory capacity were not changed by treatment. Several evaluations and considerations are discussed concerning the metabolism of some types of alpha1-antitrypsin.
Gouty arthritis developed in a twenty-one-year-old male whose karyotyping showed Trisomy 21. His serum urate level was 13.1 mg per 100 ml and his twenty-four-hour urinary uric acid excretion was 431 mg on a low purine diet. Uric acid clearance was decreased to 3.9 ml per minute. The cumulative incorporation of N15-glycine into urinary uric acid during successive seven days was 0.144 per cent, which was within the normal range. Diminished uric acid clearance may be attributed to this hyperuricaemia. The cause of gouty arthritis and Down's syndrome in the patient is discussed.
The distribution of C'3 phenotypes in 61 seropositive rheumatoid arthritis patients and 464 normal blood donors in Tokyo was examined by high-voltage agarose gel electrophoresis. The allele of the common European variant, C3(F), is absent in Japanese, but another F allels, C3(Frare), is present with a frequency of 0.025 and 0.013 in RA patients and blood donors, respectively; the difference is not statistically significant. The distribution of phenotypes for several other enzyme systems was also determined in an attempt to detect association with RA Again, no statistically significant differences were found.