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Biomedical subjects

O Igarashi

Publications and source records attributed to O Igarashi.

11 recordsLinked to original sources

Metabolism of arachidonic, eicosapentaenoic, and docosahexaenoic acids in HepG2 cells and rat hepatocytes.

The metabolism of arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) was examined in HepG2 cells, a human hepatoma cell line, and rat hepatocytes. The AA level in HepG2 cells was lower than in rat hepatocytes and incorporation of AA into HepG2 was also smaller than into rat hepatocytes. Both cells could not increase the level of cellular DHA by the addition of exogenous 22:5 (n-3); whereas, rat hepatocytes, but not HepG2 cells, increased the levels of AA from 20:3 (n-6) and EPA from 20:4 (n-3). In both cells, retroconversion of AA to 20:3 (n-6) occurred, but EPA was not retroconverted to 20:4 (n-3). These results suggested that the levels of AA and DHA in both types of cells, were regulated more severely than EPA and that the activity of fatty acid desaturation might be different between n-6 and n-3 families.

Animals

Effects of sesamin and curcumin on delta 5-desaturation and chain elongation of polyunsaturated fatty acid metabolism in primary cultured rat hepatocytes.

Effects of sesamin and curcumin on delta 5-desaturation and chain elongation of polyunsaturated fatty acid (PUFA) were studied in rat primary cultured hepatocytes. When sesamin was added to culture medium containing 20:4 (n-3), rat hepatocytes after 24 h of incubation produced 20:5 (n-3) from 20:4 (n-3), whereas when incubated with 20:3 (n-6), the metabolite by delta 5-desaturation did not accumulate, and consequently, the ratio of 20:3 (n-6)/20:4 (n-6) increased with the amount of sesamin added. Curcumin was more effective than sesamin in this respect. Both sesamin and curcumin interfered with chain elongation of PUFAs. An addition of 18:3 (n-6) or 18:4 (n-3) increased the cellular concentrations of 20:3 (n-6) or 20:4 (n-3), respectively, but the simultaneous addition of sesamin or curcumin inhibited the chain elongation of C18 acids (the fatty acids with 18 carbons) into corresponding C20 and C18 acids. Similarly, the elongation from C20 of n-3 and n-6 families to C22 was also inhibited with sesamin and curcumin. These results suggested that: 1) sesamin and curcumin inhibited delta 5-desaturation of n-6 fatty acid, but not n-3 fatty acid in rat hepatocytes; 2) curcumin was more effective than sesamin; 3) chain elongation was also inhibited by sesamin and curcumin.

Animals

Synergistic action of vitamin E and vitamin C in vivo using a new mutant of Wistar-strain rats, ODS, unable to synthesize vitamin C.

It is well known that vitamins E and C exhibit synergistic action in in vitro systems, but with regard to in vivo systems, much of the available data are confusing. To elucidate this problem we used a new mutant of Wistar-strain rats that cannot synthesize vitamin C, namely, ODS rats. Two experiments were planned: (1) during development of vitamin E deficiency, whether vitamin C could spare the consumption of vitamin E; and (2) under conditions of a regular level of vitamin E intake, whether different dose levels of vitamin C can affect vitamin E concentration in tissues. The results obtained show that with vitamin C intake, higher levels of vitamin E were deposited in tissues in both experiments. With the development of vitamin E deficiency, rats in the group with a higher dose of vitamin C deposited higher concentrations of alpha-tocopherol. With simultaneous administration of vitamin E and vitamin C to the same mutant rats, the rats in the group with a higher dose of vitamin C deposited higher levels of vitamin E in all tissues tested. Thus, we concluded that vitamin C can spare the consumption of vitamin E in vivo as well as in vitro.

Animals

The oxidation products from two kinds of tocopherols co-existing in autoxidation system of methyl linoleate.

The oxidation products of both types of mixtures of alpha-tocopherol (alpha-Toc) and gamma-tocopherol (gamma-Toc) or alpha-Toc and delta-tocopherol (delta-Toc) during autoxidation of methyl linoleate were isolated and identified. The structures of the oxidation products were characterized by UV, IR, 1H and 13CNMR, and mass spectrometry. The 5-[2-(alpha-tocopherol-5'-yl)ethyl]-alpha-tocopherylquinone, 5-[2-(alpha-tocopherol-5'-yl)ethyl]-8a-hydroxy-alpha-tocopherone, O-[8-(5-ethoxymethyl-7-methyltocol)methyl]-alpha-tocopherol were obtained from both types of the mixtures as the oxidation products derived from alpha-Toc. gamma-Toc diphenyl ether dimer (gamma-TED) and gamma-Toc biphenyl dimer (gamma-TBD) were identified from the mixture of alpha-Toc and gamma-Toc, and delta-Toc diphenyl ether dimer (delta-TED) from the mixture of alpha-Toc and delta-Toc. However, no oxidation product composed of both alpha-Toc and gamma-Toc or delta-Toc was detected in oxidation products of both types of the mixtures. These results support the facts that, at first, oxidation of alpha-Toc proceeds during autoxidation of lipids and then gamma-Toc or delta-Toc decomposes after approximate consumption of alpha-Toc.

Chromatography, High Pressure Liquid

Differentiation of acupuncture and nonacupuncture points by difference of associated opioids in the spinal cord in production of analgesia by acupuncture and nonacupuncture point stimulation, and relations between sodium and those opioids.

Antiserum of methionine-enkephalin (Met-Enk) applied intrathecally abolished acupuncture analgesia (AA) caused by low frequency stimulation of an acupuncture point (tibial muscle, APS) of rats, but antisera of leucine-enkephalin (Leu-Enk) and dynorphin (Dyn) did not. Antiserum of Dyn applied intrathecally abolished analgesia (NAA) produced by stimulation of a nonacupuncture point (NAPS) which was revealed by lesion in the analgesia inhibitory system (AIS), whereas antisera of Met-Enk and Leu-Enk did not. NAA was antagonized by the kappa-receptor antagonist, Mr2266, and analgesia was produced by the kappa-agonist, U50-488H, in the AIS lesioned rats. Potentials in the dorsal periaqueductal central gray (D-PAG) evoked by APS were antagonized by naloxone and antiserum of Met-Enk, and those in the lateral PAG (L-PAG) evoked by NAPS were antagonized by Mr2266 and antiserum of Dyn. After adrenalectomy, AA, potentials in the D-PAG, and analgesia caused by stimulation (SPA) of the D-PAG were abolished 12 hour; and NAA, potentials in the L-PAG, and SPA of the L-PAG were abolished in 24 hour. All were then restored one hour after intravenous application of 1 ml of 5% NaCl solution. AA and NAA which were augmented for several hours before their abolition after adrenalectomy were not antagonized by naloxone nor M 2266, respectively. However naloxone and Mr2266 did antagonize AA and NAA, respectively, one hour after treatment with 1 ml of 5% NaCl solution.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh

Effects of gammalinolenic acid on plasma lipoproteins and apolipoproteins.

Nineteen hypercholesterolemic patients (10 without and 9 with hypertriglyceridemia) were given evening primrose oil rich in gammalinolenic acid (GLA, 18: 3n - 6), in a placebo controlled cross-over design, over 16 weeks (8 + 8 weeks), with safflower oil as the placebo. During supplementation with evening primrose oil, dihomogammalinolenic acid (20: 3n - 6) increased in plasma lipids and red blood cells, and in subjects without hypertriglyceridemia there was a significant decrease in low density lipoprotein-cholesterol and plasma apolipoprotein B compared with the levels observed during safflower oil administration. Our results confirmed that evening primrose oil is effective in lowering low density lipoprotein in hypercholesterolemic patients.

Adult

Metabolism of gamma-linolenic acid in primary cultures of rat hepatocytes and in Hep G2 cells.

Incorporation and metabolism of gamma-linolenic acid (GLA) in both rat hepatocytes and Hep G2 cells were compared to those of oleic (OA), linoleic (LA), alpha-linolenic (LLA), and dihomo-gamma-linolenic (DGLA) acids. The incorporation of GLA into both types of cells was higher than LLA and DGLA, but lower than OA and LA. It was efficiently converted into DGLA in both types of cells and increased the concentration of DGLA. LLA was converted to a small amount of C20:4 (n-3) only in Hep G2 cells. Incubation with LA, GLA, LLA, and DGLA did not increase the concentration of arachidonic acid (AA) in both types of cells. LA. GLA, LLA, and their metabolites were incorporated into phosphatidylcholine, but only GLA and its metabolite, DGLA, were also incorporated into phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol. The coexistence of GLA and LLA during their catabolism diminished the amounts of respective metabolite in Hep G2 cells. The presence of GLA inhibited completely the formation of C20:4(n-3) from LLA. The results indicate that GLA is more effective in raising the ratio of DGLA/AA. Also, polyunsaturated fatty acids of n-3 and n-6 series have competitively catabolized in both types of hepatocytes.

8,11,14-Eicosatrienoic Acid

Oxidation products of N-methyl-2,2,7,8-tetramethyl-6-amino-chroman, a model compound of N-methyl-gamma-tocopheramine with potassium ferricyanide.

N-Methyl-2,2,7,8-tetramethyl-6-amino-chroman, a model compound of N-methyl-gamma-tocopheramine, was submitted to an oxidation study with alkaline potassium ferricyanide. As oxidative products, 2,2,7,8-tetramethyl-6-amino-chroman and dimeric (VI) were identified. Also, a trace of compound C which might be a azochroman was detected. It was concluded that an N radical formation is necessary to take the role of a biological antioxidant of N-methyl-gamma-tocopheramine.

Antioxidants

The influence of propranolol on the cardiovascular effects and plasma clearance of epinephrine.

The purpose of the present study was to determine how propranolol modifies the circulatory effects of epinephrine infused to produce plasma concentrations achieved during dental local anesthesia and to evaluate the effects of propranolol on the plasma clearance of epinephrine. The study was performed on six healthy male volunteers ranging in age from 25 to 34 yr. Five measurement series were performed on each of these subjects at the following times: pretreatment control, 15 min after the beginning of the first epinephrine infusion (10 ng/kg/min), 15 min after the cessation of the first epinephrine infusion, 3 min after the intravenous injection of propranolol 40 micrograms/kg, and 15 min after the beginning of the second epinephrine infusion. Plasma epinephrine clearance decreased to 54.7 +/- 9.3% of the control value after propranolol was given. Epinephrine showed initially a predominantly beta-adrenergic action, but this action was inhibited by propranolol. A relative alpha-dominant state may then occur, even when a routine volume of dental local anesthetic is administered to a chronic user of a nonselective beta blocker, and it is postulated that myocardial ischemia may develop in such patients.

Adult