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R K Gordon

Publications and source records attributed to R K Gordon.

42 records · Page 3Linked to original sources
PubMed1982

The effect of vitamin E deficiency on some platelet membrane properties.

The effects of alpha-tocopherol (vitamin E) deficiency on membrane properties of platelets were studied to determine if vitamin E has a measureable stabilizing role in biological membranes. Three groups of rats and three of mice were studied: two groups consisted of Fisher strain rats and one of Sprague-Dawley rats fed a Draper corn oil diet with and without high levels of supplementary vitamin E. The mice were two groups of BALB/c animals maintained on an 8% hydrogenated coconut oil diet, and one group of CBA/J mice on an 8% lard diet, in each case either deficient in or supplemented with vitamin E. The relative content of fatty acids obtained from both rat platelets and erythrocytes was unchanged by vitamin E deficiency. Depletion of vitamin E had no effect on the degree of fluorescence polarization of 1,6-diphenyl-1,3,5,-hexatriene-labeled rat platelets. No changes in hematocrit values were seen in any of the studies. The platelet count of only the vitamin E-deficient Sprague-Dawley rats was elevated with respect to vitamin E-supplemented counterparts; the others remained constant. Platelet reactivities, as measured by ADP-and thrombin-induced platelet aggregation and by the thrombin-induced changes in platelet transmembrane potential, were unaffected by vitamin E deficiency in all three groups of rats. Our results indicate that a membrane stabilizing effect of vitamin E on rat platelet or erythrocyte membrane fatty acids or on platelet response to external stimuli could not be demonstrated, nor was elevation in platelet count a general phenomenon associated with vitamin E deficiency.-Whitin, J. C., R. K. Gordon, L. M. Corwin, and E. R. Simons. The effect of vitamin E deficiency on some platelet membrane properties.

Animals↗
PubMed1981

Studies of the mode of action of vitamin E in stimulating T-cell mitogenesis.

Vitamin E stimulates mitogenesis produced by suboptimal concentrations of concanavalin A (Con A) and optimal concentrations of phytohaemagglutinin (PHA) but not that produced by optimal concentrations of Con A. In this report, fractionation of CBA/J murine spleen cells was performed to discover the vitamin-E-responsive spleen cell populations. It was found that removal of adherent cells on plastic and/or removal of Ia+ cells failed to decrease the effectiveness of vitamin E in enhancing mitogenesis. This indicated that vitamin E stimulates an Ia- cell population even in the absence of accessory cells. Another stimulatory effect of vitamin E was observed on whole spleen cells. When the latter were obtained from the mouse without washing, the vitamin enhanced mitogenesis as usual. Thorough washing of the spleen cells stimulated the response, and further stimulation by vitamin E was no longer seen. Readdition of the soluble splenic wash decreased the mitogenic response and restored the vitamin-E-enhancing effect. It was concluded that vitamin E stimulated mitogenesis of whole spleen cells by overcoming the effects of a soluble suppressor naturally occurring in the spleen cells by overcoming the effects of a soluble suppressor naturally occurring in the spleen. It was further demonstrated that vitamin E enhances mitogenesis long after commitment to and subsequent removal of Con A.

Animals↗
PubMedDate not supplied

Vasoactive intestinal polypeptides induce guinea-pig ileum contraction by causing release of endogenous acetylcholine.

Two vasoactive intestinal polypeptide (VIP) analogues were observed to induce a concentration-dependent contraction of guinea-pig ileum, which was blocked by atropine but not by tubocurarine. The analogue from guinea-pig, VIP [VIP(gp)], was the most potent inducer of ileum contraction, followed by human-porcine-rat VIP [VIP(hpr)], which differs from VIP(gp) by 4 nonpolar amino acid substitutions. VIP(1-15), composed of only the first 15 of the 28 amino acids of VIP(hpr), was without effect. The relative potency of VIP(gp), VIP(hpr), and acetylcholine was 50 to 100 times more potent in inducing contraction in ileums of which the acetylcholinesterase was inactivated by paraoxon than in the controls. The VIP analogues which induced contraction of ileum also induced secretion of endogenous acetylcholine. The secreted acetylcholine was quantified by high-performance liquid chromatography using electrochemical detection and an immobilized-enzyme column consisting of choline oxidase and acetylcholinesterase. The induction of ileum contraction by VIP(gp), from 10nM to 1 microM VIP, was correlated with the amounts of ACh secreted from ileum. VIP(hpr) induced less acetylcholine secretion than VIP(gp), and was also less potent in causing ileum contraction. VIP(1-15), even at 10 microM, caused neither acetylcholine release nor ileum contraction.

Acetylcholine↗