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S Hammarström

Publications and source records attributed to S Hammarström.

At least 163 records · Page 9Linked to original sources
PubMed1982

Transferrin receptors on mitogen-stimulated human thymus-derived lymphocytes.

The appearance of transferrin receptors on mitogen-stimulated human thymus-derived (T) lymphocytes was studied. When indirect immunofluorescence with immunoadsorbent-purified antitransferrin antibodies was used, approximately 10% of resting T cells were stained. This proportion increased to 50-80% of the cells 3-4 days after stimulation with the mitogenic lectins concanavalin A (Con A) and leucoagglutinin (La) from Phaseolus vulgaris. Almost all blast cells (greater than or equal to 90%) were positive. Cell binding experiments with 125I-labelled transferrin indicated the presence of 1-5 x 10(5) transferrin receptor molecules/cell with high avidity for transferrin (K = 2 - 12 x 10(8) l/mol). Analysis by sodium dodecyl sulphate polyacrylamide gel electrophoresis and autoradiography of cell lysates containing 125I-labelled T-cell surface components revealed two surface peptides (90 kdaltons and 80 kdaltons, reducing conditions), which selectively bound to insolubilized antitransferrin antibodies. The 90-kdalton peptide also bound to insolubilized transferrin. The 80-kdalton peptide is most probably transferrin and the 90-kdalton peptide the transferrin receptor. Unreduced transferrin receptor had a molecular weight of 180 kdalton. It is probably a glycoprotein, since it reacted with wheat germ agglutinin, La, and probably also Con A. The properties of the lymphocyte transferrin receptor are similar to those described for transferrin receptors on various in-vitro-grown transformed cells. This speaks in favour of a common receptor present on all proliferating human cells.

Concanavalin A↗
PubMed1981

Metabolism of leukotriene C3 in the guinea pig. Identification of metabolites formed by lung, liver, and kidney.

[5,6,8,9,11,12-3H6]Leukotriene C3 was converted to polar metabolites which ere excreted in feces and urine for 4-5 days after subcutaneous administration to guinea pigs. Lung homogenates converted leukotriene C3 to leukotriene D3. Liver and kidney homogenates did not catabolize leukotriene C3 appreciably due to inhibition of gamma-glutamyl transpeptidase in these tissues by endogenous glutathione. Liver and kidney homogenates metabolized [3H6]leukotriene D3 to the cysteine analog, leukotriene E3 (Bernström, K., and Hammarström, S. (1981) J. Biol. Chem. 256, 9579-9582). In addition leukotriene C3 and products of greater polarity were formed. The conversion of leukotriene D3 to leukotriene C3 was catalyzed by gamma-glutamyl transpeptidase which performed a reverse reaction due to the high tissue concentrations of glutathione. The results suggest that the degradation of leukotriene C3 to leukotriene D3 is important for the further metabolism of this leukotriene in liver and kidney.

8,11,14-Eicosatrienoic Acid↗
PubMed1981

Metabolism of leukotriene D by porcine kidney.

An enzyme from porcine kidney converted leukotriene D4 into a less polar metabolite. The structure of this compound was 5-hydroxy-6-S-cysteinyl-7,9-trans-11,14-cis-eicosatetraenoic acid (leukotriene E4). Analogous products, viz. 5-hydroxy-6-S-cysteinyl-7,9,11-eicosatrienoic acid (leukotriene E3), 5-hydroxy-6-S-cysteinyl-7,9,11-trans-14-cis-eicosatetraenoic acid (11-trans-leukotriene E4), and 5-hydroxy-6-S-cysteinyl-7,9,11,14,17-eicosapentaenoic acid (leukotriene E5) were formed from leukotrienes D3, 11-trans-D4, and D5, respectively. Leukotriene E4 induced slow reacting substance-like contractions of guinea pig ileum but was less potent (8-12 times) than leukotriene C4. The biological potency of 11-trans-leukotriene E4 was similar to that of leukotriene E4.

Animals↗
PubMed1981

Conversion of 5,8,11-eicosatrienoic acid to leukotrienes C3 and D3.

5,8,11-Eicosatrienoic acid was converted by mouse mastocytoma cells stimulated with ionophore A23187 to two slow reacting substances. These were characterized by spectroscopy and by chemical and enzymatic degradations as two geometrical isomers of 5-hydroxy-6-S-glutathionyl-7,9,11-eicosatrienoic acid (E,E,Z; leukotriene C3 and E,E,E; 11-trans-leukotriene C3). Corresponding cysteinylglycine compounds (leukotriene D3 and 11-trans leukotriene D3) were obtained from the leukotriene C3 isomers by treatment with kidney gamma-glutamyl transpeptidase. The biological effects of leukotrienes C3 and D3, on the isolated guinea pig ileum, were approximately the same as of leukotrienes derived from arachidonic acid.

8,11,14-Eicosatrienoic Acid↗
PubMed1981

Conversion of 14C-labeled eicosapentaenoic acid (n-3) to leukotriene C5.

14C-labeled eicosapentaenoic acid (n-3) was converted by mouse mastocytoma cells to 5-hydroxy-6-S-glutathionyl-7,9,11,14,17-eicosapentaenoic acid (leukotriene C5). The identification was based on comparisons with previously characterized unlabeled material by high-performance liquid chromatography, ultraviolet spectroscopy, and conversion by gamma-glutamyl transpeptidase to leukotriene D5.

Animals↗
PubMed1981

Leukotrienes promote plasma leakage and leukocyte adhesion in postcapillary venules: in vivo effects with relevance to the acute inflammatory response.

Leukotrienes B4, C4, and D4, members of a recently discovered family of substances biosynthesized from arachidonic acid, were found to have potent microvascular actions in the hamster cheek pouch. When applied topically to the vascular network, leukotrienes C4 and D4 caused an intense constriction of arterioles, being similar to angiotensin in potency in this respect. The vasoconstriction induced by leukotrienes C4 and D4 was short-lived, and it was consistently followed by a marked and dose-dependent extravasation of macromolecules from postcapillary venules. Histamine did not constrict arterioles, but it elicited leakage of plasma, although on a molar basis it was no more than 1/1000th as potent as the leukotrienes. When used in the same concentration range as leukotrienes C4 and D4, leukotriene B4 did not evoke vasoconstriction or promote plasma leakage. On the other hand, leukotriene B4 caused a conspicuous and reversible adhesion of leukocytes to the endothelium in postcapillary venules. Our findings that leukotrienes induce microcirculatory alterations in vivo, closely resembling the early events in the acute inflammatory response, imply that leukotrienes, formed in several blood-borne and tissue-bound cells, may mediate important microcirculatory adjustments to noxious stimuli.

Animals↗
PubMed1981

Formation of leukotrienes E3, E4 and E5 in rat basophilic leukemia cells.

Rat basophilic leukemia (RBL-1) cells incubated with ionophore A23187 and 5,8,11-eicosatrienoic acid produced three slow-reacting substances identified as leukotrienes C3, D3 and E3 by spectroscopic, chromatographic and enzymatic methods. 5,8,11,14,17-Eicosapentaenoic acid was similarly converted by RBL-1 cells to leukotrienes C5, D5. and E5. Leukotrienes C4, D4 and E4 were also formed in these experiments from endogenous arachidonic acid. Time-course studies, incubations with 3H-labeled leukotriene C3 and effects of acivicin [L-(alpha S, 5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid; a gamma-glutamyl transpeptidase inhibitor] indicated that leukotrienes C and D are intermediates in the formation of leukotrienes E. L-Cysteine enhanced the conversion of leukotriene C3 to leukotriene D3 and inhibited further degradation of leukotriene D3 to leukotriene E3.

8,11,14-Eicosatrienoic Acid↗
PubMed1981

Serum level of biliary glycoprotein I, a determinant of cholestasis, of similar use as gamma-glutamyltranspeptidase.

Biliary glycoprotein I (BGP I), a constituent of normal bile and serum, is a glycoprotein (mol. wt. approximately 90,000) containing about 40% carbohydrate. Serum BGP I (S-BGP I) was determined by means of a double-antibody radioimmunoassay in patients with liver and gastrointestinal disease and in healthy individuals. The serum levels of five liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase (S-ALP), gamma-glutamyltranspeptidase (S-GT), and lactic dehydrogenase), bilirubin (total and conjugated), and bile acids (cholic and chenodeoxycholic acid) were determined in parallel. Healthy individuals had 0.5 +/- 0.3 mg/l of S-BGP I (mean +/- 2 S.D.; range, 0.2-0.9 mg/l). Most patients with liver disease (chronic hepatitis, alcoholic cirrhosis, primary biliary cirrhosis) had elevated levels, up to 5-10 times the upper reference limit, whereas most patients with gastrointestinal disease (ulcerative colitis, Crohn's disease, other GI diseases) had normal values. In patients with liver disease S-BGP I was positively correlated (p less than 0.0005) to S-GT. In primary biliary cirrhosis a positive correlation (p less than 0.005) between S-BGP I and S-ALP was also obtained. All other comparisons between S-BGP I and the other liver function tests showed non-significant correlations. It is concluded that S-BGP I is a determinant of cholestasis of similar use as S-GT.

Adolescent↗
PubMed1980

Leukotrienes are potent constrictors of human bronchi.

Slow reacting substance of anaphylaxis (SRS-A) is released by various stimuli, including immunological challenge, and has long been considered an important mediator of immediate hypersensitivity reactions, such as bronchoconstriction in allergic asthma. Recently, slow reacting substances from several tissues have been identified and characterized as members of a newly discovered group of substances, the leukotrienes. Leukotrienes are generated from arachidonic acid and other polyunsaturated fatty acids in a pathway initially involving a lipoxygenase-catalysed oxygenation at C-5 (Fig. 1). This differs from the synthesis of prostaglandins and thromboxanes, where the initial transformation of arachidonic acid is catalysed by a cyclo oxygenase (Fig. 1). Recently, leukotriene C4(LTC4:5(S)-hydroxy,6(R)-S-glutathionyl-7,9-trans, 11,14-cis-eicosatetraenoic acid) and D4(LTD4:5(S)-hydroxy,6(R)-S-cysteinyl-glycyl-7,9-trans,11,14-cis-eicosatetraenoic acid) were found to have biological effects in several bioassay systems, which are strikingly similar to those previously reported for impure extracts of SRS-A. Here we report the remarkable contractile activity of both LTC4 and LTD4 on isolated human bronchi, which further emphasizes the possibility that leukotrienes are potent mediators of bronchoconstriction in man.

Arachidonic Acids↗
PubMed1980

Inhibition of leukotriene C and leukotriene D biosynthesis.

Leukotriene C4 and leukotriene D4 are slow reacting substances produced by mouse mastocytoma cells and rat basophilic leukemia cells, respectively. Serine x borate complex, an inhibitor of glutamyl transpeptidase (EC 2.3.2.2), prevented the formation of the biologically more potent leukotriene D4 and caused accumulation of leukotriene C4 in rat basophilic leukemia cell suspensions. 5,8,11-Eicosatriynoic acid, a lipoxygenase inhibitor, prevented the biosynthesis of leukotriene C4 (ID50, 5 microM) by mastocytoma cells. The results demonstrate that gamma-glutamyl transpeptidase is involved in the biosynthesis of leukotriene D4 and suggest that leukotriene C4 is formed as an intermediate.

Animals↗
PubMed1980

Leukotriene C5: a slow reacting substance derived from eicosapentaenoic acid.

Mouse mastocytoma cells incubated with ionophore A23187 and eicosapentaenoic acid (n-3) produced a slow reacting substance with different properties compared with leukotriene C4 (previously designated leukotriene C). This product was characterized by spectroscopy and enzymatic and chemical degradations to be 5-hydroxy-6-S-glutathionyl-7,9,11,14,17-eicosapentaenoic acid (leukotriene C5). Leukotriene C5 has similar biological activity on the isolated guinea pig ileum but is less potent than is leukotriene C4.

Animals↗