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Biomedical subjects

J A Olson

Publications and source records attributed to J A Olson.

At least 145 records · Page 8Linked to original sources
PubMed1988

Vitamin A and vitamin E status of rural preschool children in West Java, Indonesia, and their response to oral doses of vitamin A and of vitamin E.

Vitamin A and E status was studied in five groups (satisfactory growth, reduced growth, night blindness, Bitot's spots, and corneal xerosis) of rural Indonesian preschool children. All groups except corneal xerosis showed satisfactory weight-height ratios. Initial serum retinol values were less than 0.35 mumol/L in 34% of all children. After oral administration of 24.4 mumol vitamin A, mean serum retinol values rose from 0.42 to 0.70 mumol/L at 10 d. After oral treatment of children with 244 or 314 mumol vitamin A, mean serum retinol remained greater than 0.56 mumol/L for 165 d. Of particular note were the low mean initial serum alpha-tocopherol concentrations (6.3 mumol/L) and alpha-tocopherol-total lipid ratios (1.5 mumol/g). Total serum lipids fell in the normal range. Oral administration of 84 mumol vitamin E raised serum alpha-tocopherol and alpha-tocopherol-total-lipid ratios by 46 and 44%, respectively. Thus, vitamin E inadequacy, which impairs vitamin A absorption and storage, may well contribute to the high incidence of clinical vitamin A deficiency in West Javan children.

Administration, Oral↗
PubMed1988

A modified relative dose-response assay employing 3,4-didehydroretinol (vitamin A2) in rats.

3,4-Didehydroretinol (vitamin A2, DR, dehydroretinol), a naturally occurring analogue of retinol (vitamin A1, R), is active in vision, growth and cellular differentiation but is converted to retinol in very small amounts, if at all. When vitamin A-depleted rats were given 500 micrograms of R acetate, a naturally occurring mixture of 480 micrograms DR ester and 20 micrograms R ester or 500 micrograms DR acetate orally in corn oil, serum levels of all administered retinoids peaked between 3.5 and 5 h and then declined. When an oral dose of 600 micrograms DR/kg body wt was administered to rats with various liver reserves of vitamin A, the serum ratio of DR to R at 3.5 h was inversely related to the liver reserves of vitamin A below approximately 2 micrograms/g liver. Because the administration of DR does not affect serum R values, a single blood sample taken at 3.5 h might provide information analogous to that obtained from two blood samples in the conventional relative dose-response method.

Animals↗
PubMed1987

Chemical synthesis and growth-promoting activity of all-trans-retinyl beta-D-glucuronide.

All-trans-retinol reacts with methyl (2,3,4-tri-O-acetyl-1-bromo-1-deoxy-beta-D-glucopyran)uronate in the presence of Ag2CO3 to give the triacetate methyl ester of retinyl beta-glucuronide. Hydrolysis of this ester with sodium methylate in methanol gives retinyl beta-D-glucuronide in about 15% yield. The water-soluble retinyl beta-D-glucuronide was characterized by u.v.-visible, n.m.r. and mass spectra, by elemental analysis and by its susceptibility to hydrolysis by bacterial beta-glucuronidase. Retinyl beta-glucuronide, when administered intraperitoneally in saline (0.9% NaCl), supports well the growth of vitamin A-deficient rats.

Animals↗
PubMed1987

Recommended dietary intakes (RDI) of vitamin K in humans.

Vitamin K is essential for the formation of at least three proteins involved in blood clotting as well as of other proteins found in plasma, bone, and kidney. Vitamin K deficiency, however, primarily affects the blood clotting process. Vitamin K is provided both from the diet and from endogenous bacterial synthesis, presumably in roughly equal measure. Because intakes of 0.4 micrograms X kg-1 X d-1 (0.89 nmol X kg-1 X d-1) and probably lower intakes maintain normal clotting activities in healthy neomycin-treated adults, rounded daily recommended dietary intakes (RDI) for essentially all reference 76-kg men and 62-kg women are 45 micrograms (100 nmol) and 35 micrograms (78 nmol) phylloquinone, respectively. Newborn infants are at high risk because breast milk contains inadequate concentrations of vitamin K and their intestines are not yet colonized with vitamin K-producing bacteria. Body reserves of vitamin K are small and turnover rapidly. Hence, supplementation of infants with vitamin K is highly advisable. Increments of vitamin K during pregnancy and lactation are also suggested.

Adolescent↗
PubMed1987

Recommended dietary intakes (RDI) of vitamin C in humans.

Vitamin C is unevenly distributed throughout all body cells and fluids. A total-body pool of 900 mg (5.11 mmol) in an adult male meets the following criteria of a satisfactory vitamin C status: it is threefold higher than one that prevents scurvy, no known health advantages accrue at higher pool sizes, absorption efficiency is high and urinary loss low at appropriate intakes, and a 1-mo reserve allows for periods of low intake or stress. To maintain a suitable body pool in healthy 76-kg men and 62-kg women requires daily intakes (RDI) of 40 mg (227 mumol) and 30 mg (170 mumol), respectively. Reasons for not increasing RDI values to enhance iron absorption and to prevent nitrosamine formation are given. The specific association of normal intakes of dietary vitamin C with cancer is very weak and not quantifiable. Advisable intakes for children, pregnant and lactating women, and the elderly are considered. The present recommendations are in better accord with current information than are the 1980 RDA values.

Adolescent↗
PubMed1987

Recommended dietary intakes (RDI) of vitamin A in humans.

Mean and median dietary intakes of vitamin A in the US are approximately 1000 and 624 retinol equivalents, respectively. In this paper a satisfactory vitamin A status is defined as a total-body pool that provides adequate vitamin A to meet all known physiological needs and a reserve for 4 mo on low intakes or during stress. Mean dietary intakes required to maintain an adequate body pool (ie, 20 micrograms vitamin A/g liver [0.07 mumol/g]) in reference 76-kg men and 62-kg women are 506 and 413 micrograms retinol, respectively. Recommended dietary intakes (RDI) for nearly all reference men and women are 700 micrograms and 600 micrograms, respectively. Vitamin A needs in infants, children, the elderly, and pregnant and lactating women are quantified. The toxicity of vitamin A in early pregnancy, for which a safe intake level is not known, is stressed. On many grounds these suggested lower RDI values are preferable to the 1980 RDA values.

Adolescent↗
PubMed1987

Relative amount and ester composition of vitamin A in rat hepatocytes as a function of the method of cell preparation and of total liver stores.

The aim of this study was to determine the cellular distribution of vitamin A in the liver of adult, well-nourished Sprague-Dawley rats with different stores of this vitamin. Three groups of three rats each were fed AIN-76 diet. Each group received an oral supplement of either 0, 2, or 12 mg of retinol. Retinol and retinyl esters were measured in the whole liver, in hepatocytes isolated either by gravity sedimentation or by centrifugal elutriation, and in the supernatant solution recovered after hepatocyte sedimentation. Dietary supplementation with vitamin A increased the liver stores from 138 to 390 micrograms/g. A mean of 5% of the liver vitamin A was found in hepatocytes isolated by centrifugal elutriation. This percentage tended to decrease as liver vitamin A increased. In contrast, a mean of 38% of total liver vitamin A was found in hepatocytes isolated by gravity sedimentation over a threefold range of liver reserves. Whereas the retinol concentration in hepatocytes remained constant, the percentage of total vitamin A as retinyl esters, which accounted for more than 96% of the total vitamin A, increased as liver stores increased. The retinyl ester composition was similar in all three groups, major esters being palmitate (76-82%), stearate (9-12%), oleate (5-7%), and linoleate (3-4%). Over a threefold range of liver vitamin A concentrations in well-nourished rats, therefore, we estimate that only 10-20% of the total vitamin A in liver is present in the parenchymal cells.

Animals↗
PubMed1987

Factors influencing the level and interanimal variability of retinyl ester hydrolase activity in rat liver.

Retinyl ester hydrolase activity was studied in 25 7-wk-old rats that had been previously fed no vitamin A for 1 wk and then were fed 0, 5, 24, 60 or 240 micrograms retinol/d for 2 wk. This treatment produced rats with vitamin A reserves from depleted to normal (0.03 to 184 micrograms/g) and serum retinol concentrations of 4-67 micrograms/dl. Hydrolase activity in liver homogenates was optimal when assayed with 275 mM CHAPS (3-[(3-cholamidopropyl) dimethylammonio]-1-propanesulfonate), 2 mg/ml Triton X-100 and 5 mM retinyl palmitate at pH 7.0. By use of these concentrations and conditions, retinyl ester hydrolase activity displayed relatively low interanimal variability (fivefold). Furthermore, activity was independent of serum or liver vitamin A concentrations. When CHAPS in the assay was replaced with equimolar sodium cholate, or with reduced concentrations of CHAPS and retinyl palmitate, retinyl ester hydrolase activity was more variable, i.e., 37- and 23-fold, respectively. Furthermore, in the latter case, hydrolase activity was threefold higher in rats with liver vitamin A reserves less than 10 micrograms/g. Thus, the type and concentration of bile salt used to assay retinyl ester hydrolase affect its interanimal variability. Furthermore, hydrolase activity measured in reduced concentrations of substrate and detergent is elevated in rats with low liver reserves of vitamin A.

Animals↗
PubMed1987

A marginal vitamin A status alters the distribution of vitamin A among parenchymal and stellate cells in rat liver.

The aim of this study was to determine whether the distribution of vitamin A between parenchymal and stellate cells in rats with low vitamin A liver reserves is different from that observed in rats with adequate reserves. Retinol and retinyl esters were quantitated in parenchymal and stellate cells of the liver of three groups (n = 3) of adult Sprague-Dawley rats with mean total liver vitamin A reserves of 1.2, 14.5 and 28.9 micrograms retinol/g fresh liver for groups 1, 2 and 3, respectively. The amount of vitamin A per 10(6) cells was similar in parenchymal and stellate cells of group 1, whereas in groups 2 and 3, a much higher amount was found in stellate cells (11-fold and 27-fold higher, respectively). In group 1, 83% of the liver vitamin A was present in parenchymal cells. As liver stores rose, however, a progressively greater amount was stored in stellate cells. In group 3, 82% of the liver vitamin A was found in stellate cells. In groups 2 and 3, 87-91% of the vitamin A was found as retinyl ester, whereas in group 1, 52% was found as retinol. The retinyl ester composition was similar in parenchymal and stellate cells, major esters being palmitate (84%) and stearate (10%), with smaller amounts of oleate (2.5%) and other esters. Thus, in rats with low liver vitamin A reserves, most of the liver vitamin A is found in parenchymal cells.

Animals↗
PubMed1987

Effects of retinoid beta-glucuronides and N-retinoyl amines on the differentiation of HL-60 cells in vitro.

Retinoyl beta-glucuronide and retinyl beta-glucuronide, which are naturally occurring water-soluble metabolites of vitamin A, induce the granulocytic differentiation of HL-60 cells in vitro, as evidenced by an increased reduction of nitroblue tetrazolium. The relative effectiveness of various retinoids in differentiation is retinoic acid greater than retinoyl beta-glucuronide greater than retinyl beta-glucuronide. Under the selected assay conditions, retinol, hydroxyphenyl-retinamide, retinamide, and N-retinoyl-phenylalanine are essentially inactive in differentiation. At concentrations of retinoids from 10(-9) to 10(-5) M, cell viability was best with the retinoid beta-glucuronides and retinamide, less with retinoic acid and retinol, and poorest with the N-retinoyl aromatic amines. Cellular growth was depressed only slightly by retinyl beta-glucuronide and retinamide, but to a greater degree by the other derivatives. Retinoyl beta-glucuronide was hydrolyzed in part to retinoic acid, whereas retinyl beta-glucuronide was cleaved to retinol, if at all, at a very slow rate. Under the selected assay conditions, retinoic acid and the retinoid beta-glucuronides primarily induce the differentiation of HL-60 cells, whereas the N-retinoyl aromatic amines show cytotoxicity.

Cell Differentiation↗
PubMed1987

Altered plasma membrane phospholipid organization in Plasmodium falciparum-infected human erythrocytes.

The intraerythrocytic development of the malaria parasite is accompanied by distinct morphological and biochemical changes in the host cell membrane, yet little is known about development-related alterations in the transbilayer organization of membrane phospholipids in parasitized cells. This question was examined in human red cells infected with Plasmodium falciparum. Normal red cells were infected with strain FCR3 or with clonal derivatives that either produce (K+) or do not produce (K-) knobby protuberances on the infected red cells. Parasitized cells were harvested at various stages of parasite development, and the bilayer orientation of red cell membrane phospholipids was determined chemically using 2,4,6-trinitrobenzene sulphonic acid (TNBS) or enzymatically using bee venom phospholipase A2 (PLA2) and sphingomyelinase C (SMC). We found that parasite development was accompanied by distinct alterations in the red cell membrane transbilayer distribution of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS). Increases in the exoplasmic membrane leaflet exposure of PE and PS were larger in the late-stage parasitized cells than in the early-stage parasitized cells. Similar results were obtained for PE membrane distribution using either chemical (TNBS) or enzymatic (PLA2 plus SMC) methods, although changes in PS distribution were observed only with TNBS. Uninfected cohort cells derived from mixed populations of infected and uninfected cells exhibited normal patterns of membrane phospholipid organization. The observed alterations in P falciparum-infected red cell membrane phospholipid distribution, which is independent of the presence or absence of knobby protuberances, might be associated with the drastic changes in cell membrane permeability and susceptibility to early hemolysis observed in the late stages of parasite development.

Erythrocyte Membrane↗
PubMed1987

Use of 3,4-didehydroretinol to assess vitamin A status in rats.

The acetate and palmitate esters of 3,4-didehydroretinol (DR; vitamin A2 alcohol) have been synthesized and characterized. When administered orally in corn oil to female rats, DR was present in the serum as the alcohol, but primarily as esters in the liver. As total stores of retinol (R; vitamin A1 alcohol) decrease, the ratio of DR to R in the serum markedly increases. The ratio of DR to R in serum was greater than 0.27 at liver vitamin A1 palmitate values of less than 3 micrograms/g, 0.05-0.14 at 3-19 micrograms/g, and less than 0.04 at greater than or equal to 20 micrograms/g. Thus, the ratio of DR to R in the serum at a suitable interval after the administration of dehydroretinyl acetate may aid in assessing marginal vitamin A status. DR was not demonstrably converted to R in these studies.

Animals↗
PubMed1986

Properties of liver retinyl ester hydrolase in young pigs.

A new sensitive method for the assay of retinyl ester hydrolase in vitro was developed and applied to liver homogenates of 18 young pigs with depleted-to-adequate liver vitamin A reserves. Radioactive substrate was not required, because the formation of retinol could be adequately quantitated by reversed-phase high-performance liquid chromatography. Optimal hydrolase activity was observed with 500 microM retinyl palmitate, 100 mM 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate, and 2 mg/ml Triton X-100 at pH 8.0. The relative rates of hydrolysis of six different retinyl esters by liver homogenate were: retinyl linolenate (100%), myristate (99%), palmitate (47%), oleate (38%), linoleate (31%), and stearate (29%). The enzyme was found primarily in the membrane-containing fractions of liver (59 +/- 3%, S.E.) and kidney (76 +/- 3%), with considerably lower overall activity in kidney (57-375 nmol/h per g of tissue) than in liver (394-1040 nmol/h per g). Retinyl ester hydrolase activity in these pigs was independent of serum retinol values, which ranged from 3 to 24 micrograms/dl, and of liver vitamin A concentrations from 0 to 32 micrograms/g. Pig liver retinyl ester hydrolase differs from the rat liver enzyme in its substrate specificity, bile acid stimulation, and interanimal variability.

Animals↗
PubMed1986

Separation of retinyl esters by non-aqueous reversed-phase high-performance liquid chromatography.

Rapid separation and sensitive quantitation of vitamin A esters can be achieved by use of an acetonitrile-dichloromethane (80:20) mobile phase with a 5-microns C18 column (15 cm X 4.6 mm) and absorbance detection at 325 nm. Either a Waters Resolve or a Rainin Microsorb column was used satisfactorily. Retinyl palmitate is eluted at about 7 min (capacity factor, k' = 5.5) at a flow-rate of 1.5 ml/min; retinyl palmitate and retinyl oleate, which are usually difficult to separate, are well resolved (resolution 1.2). Sensitivity (at a signal-to-noise ratio of 10:1) is 8 pmol retinyl palmitate (equivalent to 2.5 ng retinol). Quantitation of total retinyl esters is identical to that determined by a gradient high-performance liquid chromatographic technique over the range 30-1000 ng retinyl esters. Retinyl ester peaks in rat liver extracts were identified by their characteristic light absorption spectra, susceptibility to saponification, and by co-chromatography with authentic standards. Nine vitamin A ester peaks were identified and quantitated in rat liver extracts. A 10-microns Whatman Partisil 10/25 ODS-2 column was used with the same mobile phase to obtain partial resolution of retinyl esters (resolution 1.05 between retinyl oleate and retinyl palmitate; k' = 11.0 for retinyl palmitate) and improved retention for retinol (k' = 2.5, compared with k' = 0.6 for retinol on the 5-microns column).

Animals↗
PubMed1986

Some thoughts on the relationship between vitamin A and cancer.

Retinoids clearly show both prophylactic and therapeutic effects against many kinds of neoplasm. Vitamin A deficiency and vitamin A excess, which are very different states clinically and metabolically, should be separately considered relative to carcinogenesis. The anticancer effects of retinoids and related compounds may be more closely related to their chemical structure than to their similarity to the structure and function of vitamin A. Retinoids act on cells and tissues in a number of ways. Although many interesting ideas have been proposed to clarify their mode of action, no single hypothesis adequately explains their many molecular interactions and responses. Investigation of early molecular interactions between retinoids and cells and the subsequent metabolism of retinoids in neoplastic and normal cells may aid in the clarification of their action as antineoplastic agents.

Animals↗
PubMed1986

Acyl coenzyme A:retinol acyltransferase activity and the vitamin A content of polar bear (Ursus maritimus) liver.

Acyl coenzyme A:retinol acyltransferase activity was identified in the microsomes from a polar bear liver. The highest rate of in vitro retinol esterification was 821 pmol/min/mg microsomal protein. The in vitro esterification rate displayed a small dependence upon the concentration of exogenous protein (bovine serum albumin) and even less on the concentration of sulfhydryl-reducing agent (dithiothreitol). Vitamin A was present in the liver at a concentration of 8050 micrograms/g tissue, with 98% of the vitamin in its ester form. Retinyl palmitate was 37.3% of the total liver retinyl esters, while retinyl oleate represented 20.9%, stearate 12.8%, and linoleate 7.7%.

Acyltransferases↗