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Biomedical subjects

M Mino

Publications and source records attributed to M Mino.

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

Tocopherol concentrations in platelets in children.

To determine the normal range of platelet tocopherol concentrations in childhood, 158 healthy children, 3 months to 15 years old, including 81 males and 77 females were examined and this population was compared with adults. In children, the mean platelet tocopherol concentration was 0.17 micrograms/mg protein, ranging from 0.07 to 0.39 micrograms/mg protein, with a nearly logarithmic distribution. Levels of less than 0.10 micrograms/mg protein were found in only 4 of the 158 subjects. This level may be too low in platelet concentrations for this population of children. Platelet and plasma tocopherol concentrations, and the ratio of plasma tocopherol to total lipids (tocopherol/lipid ratio) in children, excluding the infant group of less than 1 year old, were lower than those in adults. The findings from this population were quite consistent with those of a population previously investigated, with respect to the distribution of plasma and RBC tocopherol concentrations and the tocopherol/lipid ratio. The tocopherol concentrations in plasma, RBCs, and platelets in the infant group were higher than those in the other children's groups (more than 1 year old), and those concentrations were comparable to the adult ones. This may reflect the higher intake of alpha-tocopherol from the prepared formulas containing more than 1,000 micrograms/dl.

Adolescent↗
PubMed1987

Free-radical chain oxidation of rat red blood cells by molecular oxygen and its inhibition by alpha-tocopherol.

The oxidation of rat red blood cells (RBC) by molecular oxygen was performed in an aqueous suspension with an azo compound as a free-radical initiator. The RBC were oxidized at a constant rate by a free-radical chain mechanism, resulting in hemolysis. The extent of hemolysis was proportional to the concentration of free radical. alpha-Tocopherol in RBC membranes suppressed the oxidation and hemolysis to produce an induction period. Tocopherol was constantly consumed during the induction period, and hemolysis developed when tocopherol concentrations fell below a critically low level. Among the membrane lipids, phosphatidylethanolamine, phosphatidylserine, and arachidonic acids were predominantly oxidized in the absence of tocopherol. In the presence of tocopherol, however, such lipid changes were suppressed during a 120-min incubation even when hemolysis started. Membrane proteins as well as lipids were oxidized. The formation of proteins with high molecular weight and concomitant decrease of the low-molecular-weight proteins were observed on gel electrophoresis with the onset of hemolysis. This study clearly showed the damage of RBC membranes caused by oxygen radical attack from outside of the membranes, and suggested that membrane tocopherol even below a critically low level could suppress lipid oxidation but that it could not prevent protein oxidation and hemolysis.

Amidines↗
PubMed1987

Glucose tolerance factor stimulates 3-O-methylglucose transport into isolated rat adipocytes.

Glucose tolerance factor partially purified from yeast extract powder stimulated [U-14C]-D-glucose uptake to a level 5.6 times greater than the basal level in the absence of insulin in isolated adipocytes prepared from rats fed with normal laboratory chow. The factor also stimulated 3-O-methylglucose transport 2.2-fold from the basal level in the absence of insulin, but not in the presence of 8 nM insulin. Kinetic analysis revealed that glucose tolerance factor increased 3-O-methylglucose transport by decreasing the Ks value for 3-O-methylglucose with little change in the Vmax.

3-O-Methylglucose↗
PubMed1987

A simple fluorometric method to discriminate adriamycin-resistant subline from adriamycin-sensitive parental P388 murine leukemia cell line.

A fluorometric method to estimate adriamycin accumulation in cells was used to discriminate adriamycin- and vincristine-resistant sublines from sensitive parental P388 murine leukemia cells. It was easily checked that adriamycin accumulation was lower in the adriamycin- and vincristine-resistant cells than in the sensitive ones. With this method we found that tamoxifen as well as diltiazem increased adriamycin accumulation in the resistant cells to a level similar to that in the sensitive ones. The effect of progesterone was much less.

Animals↗
PubMed1986

Absence of argininosuccinate lyase protein in the liver of two patients with argininosuccinic aciduria.

The enzyme defects in two cases of argininosuccinic aciduria were examined at the molecular level by enzymatic and immunological methods. No argininosuccinate lyase activity was detected in the liver or erythrocytes of either patient nor in the kidney or brain of one of the patients even in the presence of high concentrations of the substrate. The titration curve of antiserum to human argininosuccinate lyase with the liver extract from a control subject was not affected by the addition of the liver extracts from one of the patients. Double immunodiffusion analysis revealed a single precipitin line between the purified antiserum and the liver extract from a control, but no precipitin lines between the antisera and the liver extracts from the two patients. These results indicate a complete or almost complete defect of an immunologically cross-reactive material in the liver of the patients.

Amino Acid Metabolism, Inborn Errors↗
PubMed1986

Hemolysis and membrane lipid changes induced by xanthine oxidase in vitamin E deficient red cells.

A procedure to induce hemolysis by the hypoxanthine-xanthine oxidase reaction was developed and applied to vitamin E deficient red blood cells (RBCs) in rats. The reaction system was as follows: 0.16 mM hypoxanthine, 0.05 U/ml xanthine oxidase in 2.5% RBC suspensions with an isotonic buffer (pH 7.4) containing 10 mM phosphate buffer and 125 mM saline (277 mOsm). Hemolysis was observed to depend on the vitamin E concentrations in the RBCs. Hemolysis was inhibited by catalase but not by SOD. After the reaction with vitamin E deficient RBCs, an increase in TBARS in the aqueous phase of the reaction mixture was observed. This accompanied the increase in fluorescent substances in the lipid extracts, in association with a significant decrease in the PE and PS of the RBCs, and a decrease in arachidonic acid in membrane lipids. The above changes were almost completely inhibited by tocopherol incorporated into vitamin E deficient RBCs.

Animals↗
PubMed1986

Membrane-to-membrane transfer of tocopherol in red blood cells.

The direct cell-to-cell transfer of tocopherol between red blood cells (RBCs) was examined. Two kinds of RBCs were provided; 1) Tocopherol-deficient ones showing complete dialuric acid-hemolysis and 2) tocopherol-supplemented ones showing no dialuric acid-hemolysis. The two kinds of RBCs were mixed and incubated with gentle swirling in a buffer solution. If no tocopherol transfer occurred between the two kinds of RBCs in the cell suspensions, hemolysis should not change during incubation because hemolysis is limited only in the -deficient cells in the suspensions. However, it was actually observed that when RBCs with adequate amounts of tocopherol were incubated with tocopherol-deficient RBCs, dialuric acid-induced hemolysis decreased during a 3-h incubation period. Contrarily, when an inadequate amount of tocopherol constituting a limiting level for inhibition of hemolysis, existed in RBCs which were mixed with -deficient ones, hemolysis increased after incubation. This indicates that tocopherol is transferred from the tocopherol-rich RBCs to the -deficient RBCs. The transfer was greater as the hematocrit of cell suspensions increased. Gum arabic contained in the suspensions inhibited the transfer, while bromelain (a protease which lowers the electric charge on the cell surface) increased it. These findings indicate that the transfer of tocopherol is related to the frequency of collision between cells.

Animals↗
PubMed1986

Free radical chain oxidation and hemolysis of erythrocytes by molecular oxygen and their inhibition by vitamin E.

Erythrocytes of vitamin E-deficient rats and normal rats were oxidized at 37 degrees C by molecular oxygen using a free radical initiator. The erythrocytes were oxidized by a free radical chain mechanism with kinetic chain length considerably larger than 1 and resulted in hemolysis. Vitamin E suppressed both oxidation and hemolysis, but the extent of hemolysis was determined primarily by the extent of oxidation independent of the presence or absence of vitamin E.

Amidines↗
PubMed1986

An evaluation of nutritional status of vitamin E in pregnant women with respect to red blood cell tocopherol level.

Changes in RBC tocopherol level as an index for vitamin E status were studied in relation to plasma levels of tocopherol and lipids during pregnancy. Plasma tocopherol levels increased gradually and significantly during gestation. The changes depended on changes in total lipids in plasma, of which an increase in triglycerides was most predominant. A similar increase was shown in beta-lipoprotein levels, while HDL-cholesterol did not show any significant change. The ratio of plasma tocopherol to plasma total lipids, proposed as the best index for vitamin E status by Horwitt, remained unchanged during gestation, while RBC tocopherol levels somewhat decreased during the last trimester. The result indicates that tissue tocopherol available for biological function in the biomembrane may decrease due to hyperlipemia during gestation, as reflected in RBC tocopherol change.

Adult↗
PubMed1985

Red blood cell tocopherol and liver tocopherol in hyperlipemic rats as compared with plasma tocopherol.

In rats with hyperlipemia induced by Triton WR-1339, changes in tocopherol concentrations in plasma and RBC were compared with those in the liver and its subcellular fractions, microsomes and mitochondria. After daily injection with Triton, plasma total lipids at 3 days and 7 days, respectively, showed elevations 6.5 times and 15 times as high as those in the control rats, and triglycerides showed the most predominant elevation. With the hyperlipemia, the concentrations of tocopherol in RBC and the subcellular fractions decreased, as plasma lipids and plasma tocopherol increased, while no change occurred in tocopherol concentrations in liver homogenates. The changes in the ratio of tocopherol to total lipids in plasma coincided with changes in tocopherol concentrations in the RBC and subcellular fractions.

Animals↗
PubMed1985

Red blood cell tocopherol concentrations in a normal population of Japanese children and premature infants in relation to the assessment of vitamin E status.

To determine the normal range of red blood cell (RBC) tocopherol as an assessment of vitamin E nutritional status, 261 apparently healthy children, 3 to 16 years old, including 160 males and 101 females, were investigated and this population was compared with premature infants and adults. In the children, the mean plasma tocopherol was 682 micrograms/100 ml, ranging from 309 to 1,442 micrograms/100 ml. Plasma tocopherol expressed in terms of total lipids (tocopherol/lipid ratio) was generally within accepted value (greater than 0.8). Only one had a value below 0.8. The mean RBC tocopherol was 179 micrograms/100 ml packed cells ranging from 79 to 320 micrograms/100 ml. When the cumulative percentage frequency was examined, the value of 115 micrograms/100 ml corresponded to the fifth percentile of the population of RBC. Thirteen of 90 premature infants (14.4%) less than 24-hours-old and 9 of 48 at 7 days of age (18.8%) had values of less than 115 micrograms/100 ml packed RBCs, while on the basis of the tocopherol/lipid ratio, 44.8% of the infants less than 24-hours-old and 22.2% of those 7 days old had values below 0.8. No adult was below the accepted values of either RBC tocopherol or the tocopherol/lipid ratio.

Adolescent↗
PubMed1985

Comparative changes in plasma and RBC alpha-tocopherol after administration of dl-alpha-tocopheryl acetate and d-alpha-tocopherol.

Changes in plasma and RBC alpha-tocopherol after intravenous and oral administration of dl-alpha-tocopheryl acetate were investigated using vitamin E-deficient rats and were compared with those following the administration of d-alpha-tocopherol, which is the most active and natural form of tocopherol. Intravenous administration: By the administration of dl-tocopheryl acetate, the elevated plasma tocopherol levels were higher at 6 h than those elevated by d-tocopherol, but the RBC tocopherol was lower 6 h after the infusion of dl-tocopheryl acetate than after d-tocopherol infusion. The tocopheryl acetate incorporated into the RBCs remained for 24 h after the administration of tocopheryl acetate, the acetate then becoming undetectable in plasma. Oral administration: The tocopherol elevated in plasma and RBC was only the alpha-form and not tocopheryl acetate. In both plasma and RBCs, tocopherol levels were higher after the administration of d-tocopherol than after dl-tocopheryl acetate administration, and more was found in RBCs.

Administration, Oral↗
PubMed1985

Changes in cell proliferation kinetics in the mouse cerebellum after total asphyxia.

This study was undertaken to investigate the effects of neonatal asphyxia on brain development, with special reference to the kinetics of neuronal proliferation by using autoradiography. For 30 minutes, two-day-old suckling mice, Jcl:ICR strain, were put into a chamber which was constantly flushed with 100% CO2 gas. After the exposure to asphyxia, 29% of the mice survived. Cell cycle studies were carried out at two days and at seven days on the external matrix cells, the precursor of the granule cells, at the external granular layer of the cerebellum from CO2-exposed and control mice by 3H-thymidine autoradiography. At two days the generation time of the control mice was about 15 hours, whereas that of the asphyxiated mice was about 17 hours. The prolongation of the generation time in the asphyxiated mice was caused mainly by a delay in the G2 phase. This prolongation was apparent for about five days and thereafter growth caught up. These results suggest that neonatal asphyxia has an adverse effect on cerebellar neuronal proliferation that may revert to normal spontaneously in older animals.

Animals↗
PubMed1985

Relationship between red blood cell and liver tocopherol concentration after administration and depletion of vitamin E.

As the assessment of the nutritional status of vitamin E, the validity of red blood cell (RBC) tocopherol concentration was examined in relation to tocopherol concentration in the liver and in its subcellular fractions. When 10 mg/kg of dl-alpha-tocopherol was injected intramuscularly to vitamin E deficient rats, plasma tocopherol reached a maximum level earlier than did RBC tocopherol and liver tocopherol. However, as the correlation in tocopherol concentrations between RBC and plasma and between RBC and tissue homogenate or its subcellular fractions was examined with respect to all the values examines during the study courses, a moderately close correlation was observed between RBC and liver tissue and between RBC and the subcellular fractions while a lack of correlation was found between RBC and plasma. When rats sufficient in vitamin E were depleted for 8 weeks by a vitamin E deficient diet, tocopherol concentrations decreased in a similar pattern in the plasma, RBC, and liver and its subcellular fractions. In this case, a very close correlation in the tocopherol concentrations was observed between RBC and other subjects, i.e., the plasma, liver homogenate and its subcellular fractions.

Animals↗