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At least 883 records · Page 49Linked to original sources
PubMed1969

Ascorbic acid and copper in linoleate oxidation. I. Measurement of oxidation by ultraviolet spectrophotometry and the thiobarbituric acid test.

The UV absorption method and the thiobarbituric acid (TBA) test for oxidation of an aqueous suspension of linoleate were compared. The absorption method depends on the formation of hydroperoxides having conjugated double bonds that absorb strongly at 233 nm. The absorption at 233 nm increased markedly during oxidation of linoleate catalyzed by either ascorbic acid or cupric ions. The concentration of ascorbic acid in the reaction mixture was also measured by UV absorption at 265 nm and pH 7.0. Color development in the TBA test also increased markedly with the extent of oxidation of linoleate. When ascorbic acid was the catalyst, UV absorption detected early stages of oxidation with greater sensitivity than the TBA test. The reverse was true when Cu(++) was the catalyst. In general, the relation between the two procedures will depend on whether copper is present when the TBA test is made.

Alkenes↗
PubMed1983

Potential cerebral perfusion agents: synthesis and evaluation of a radioiodinated vinylalkylbarbituric acid analogue.

A new iodinated barbiturate has been prepared. Treatment of 5-chloropentyne and propargyl bromide with diethyl 2-ethyl-2-sodiomalonate (DESM) provided diethyl 2-ethyl-2-(1-pentyn-5-yl)malonate (3) and diethyl 2-ethyl-2-propargylmalonate (4), respectively. Similar condensation of DESM with (E)-(5-iodo-1-penten-1-yl)boronic acid (9) or the reaction of catecholborane with 3 provided diethyl (E)-2-ethyl-2-(1-borono-1-penten-5-yl)malonate (8). The direct sodium iodide-chloramine-T iodination of 8 or the treatment of (E)-1,5-diiodo-1-pentene (10) with DESM provided diethyl (E)-2-ethyl-2-(1-iodo-1-penten-5-yl)malonate (11). The condensation of functionalized malonates 3, 4, and 11 with urea in the presence of a base provided the corresponding barbiturates, 5-ethyl-5-(1-pentyn-5-yl)-(5), 5-ethyl-5-propargyl- (6), and (E)-5-ethyl-5-(1-iodo-1-penten-5-yl)barbituric acid (12), respectively. (E)-6-(Ethoxycarbonyl)-1-iodo-1-octene-6-carboxylic acid (13) was isolated as the hydrolytic byproduct of 11. Compound 13 decarboxylated under vacuum to provide ethyl (E)-1-iodo-1-octene-6-carboxylate (14). The 125I-labeled congeners of 12 and 13 were synthesized in the same manner and evaluated in rats. The barbiturate 12 exhibited significant brain uptake (approximately 1% dose after 5 min), demonstrating that iodinated barbiturates freely cross the intact blood-brain barrier.

Animals↗
PubMed1984

gamma-Aminobutyric acid activation of 36Cl- flux in rat hippocampal slices and its potentiation by barbiturates.

gamma-Aminobutyric acid (GABA) increases the rate of 36Cl- efflux from preloaded rat hippocampal slices in a dose-dependent manner (EC50: 400 microM). This action has the pharmacological specificity expected of activation of GABA receptors in that it is mimicked by the agonists muscimol and 3-aminopropanesulfonic acid, and blocked by the antagonists bicuculline and picrotoxinin. GABA uptake inhibitors, nipecotic acid and 2,4-diaminobutyric acid, fail to increase 36Cl- flux. Pentobarbital produces a dose-dependent activation (EC50 = 1.5 mM) of 36Cl- efflux with maximal response greater than that of GABA. The effect of pentobarbital can be mimicked by 1,3-dimethylbutylbarbiturate, secobarbital, (+)hexobarbital but not (-)hexobarbital, and is blocked by bicuculline and picrotoxinin. Pentobarbital and the other active barbiturates also potentiate the action of GABA. Phenobarbital does not have any effect independently or in combination with GABA. It is suggested that GABA increases 36Cl- permeability by activation of a postsynaptic receptor which is in turn functionally coupled to a barbiturate receptor.

Animals↗
PubMed1981

Barbiturate attenuation of brain free fatty acid liberation during global ischemia.

To find a biochemical basis for the increased tolerance of the brain to anoxia during barbiturate anesthesia, we studied whole-brain free fatty acids (FFA) at various times after decapitation of awake and pentobarbital-anesthetized rats. Post-decapitation, the brains were kept at 37 degrees C for 1 to 60 min before freezing in liquid N2. Nonischemic brains were frozen in liquid N2, using a rapid sampling technique. Whole-brain arachidonic, stearic, oleic, linoleic, and palmitic acids were quantitated by gas-liquid chromatography. In unanesthetized, nonischemic brain, total FFA was 1226 +/- 121 nmol/g brain (n = 12) and was unaffected by pentobarbital anesthesia (1126 +/- 86 nmol/g brain, n = 11), except for a reduction in arachidonic acid. Total FFA in unanesthetized and pentobarbital-anesthetized rats transiently declined between 0 and 1 min of ischemia, and then rose linearly for up to 60 min, with consistently lower values in pentobarbital-treated rats, the greatest attenuation being that of arachidonic and stearic acid liberation. Brain FFA liberation during global ischemia is the first known biochemical variable directly correlated with the duration (i.e., severity) of global ischemia. The attenuation of brain FFA liberation and especially of arachidonic and stearic acids may be the biochemical basis of barbiturate attenuation of ischemic brain injury.

Animals↗
PubMed1969

Ascorbic acid and copper in linoleate oxidation. 3. Catalysts in combination.

In promoting oxidation of 0.02 m potassium linoleate in a buffered (pH 7.0) aqueous dispersion at 37 degrees C, ascorbic acid at low concentrations (1.8 x 10(-6) and 1.8 x 10(-5) m) in combination with copper (1.3 x 10(-7) to 1.3 x 10(-3) m) had greater catalytic activity than the additive activity of the two catalysts individually. Possible explanations for the enhanced catalysis include reduction of copper by ascorbic acid to the cuprous form, increased concentration of semidehydroascorbic acid radical, and formation of a metal-ascorbic acid-oxygen complex. Some combinations of ascorbic acid (1.8 x 10(-4) and 1.8 x 10(-3) m) and copper (1.3 x 10(-6) and 1.3 x 10(-3) m) inhibited the formation of conjugated dienes but not the oxidation of ascorbic acid, and caused rapid loss of part of the conjugated dienes that were already present. It is suggested that free-radical inhibitors formed by the combination of catalysts inhibit initiation of lipid oxidation but not copper-catalyzed oxidation of ascorbic acid. Effects of the inhibitory combinations on changes in UV absorption by conjugated dienes, and absorbance in the TBA test, indicate the presence of at least two conjugated dienes that differ in stability.

Alkenes↗
PubMed1980

[Reciprocal action between caffeine, other stimulants and drugs].

Caffeine is ingested not only with beverages as coffee, tea, coca-cola but also in form of many analgetic drugs. Therefore interactions of this substance with other biologically active substances and drugs should be expected, and the knowledge of these would be of practical importance. The interactions between caffeine and alcohol, smoking, salicylic acid, phenacetin, barbiturates, and theobromine are described.

Analgesics↗