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At least 19 recordsLinked to original sources
PubMed1979

Acute metabolic interaction of ethanol and drugs.

Addition of ethanol in vitro was found to inhibit the microsomal metabolism of a variety of drugs such as meprobamate, aminopyrine, pentobarbital and zoxazolamine. In all cases, a mixed type of inhibition was obtained. When the concentration of alcohols of different chain lengths required to inhibit 50% of the metabolism of drugs was plotted against their corresponding octanol-water partition coefficients (Po/w) it was found that the inhibitory potency of alcohols is linearly related to the partition coefficients, with a slope of 0.98. In vivo acute administration of ethanol also resulted in decreased whole body metabolism of meprobamate, aminopyrine, pentobarbital, zoxazolamine and aniline. In vitro addition of pentobarbital, phenobarbital and meprobamate had no significant effect on ethanol metabolism by liver slices. Acute pretreatment with these drugs also had no effect on the rate of ethanol metabolism in vivo as measured in the whole body or as estimated from the rate of decrease of blood ethanol concentration. It appears therefore that acute metabolic interaction of ethanol and drugs is a one sided phenomenon, i.e. ethanol inhibits drug metabolism, whereas drugs do not inhibit ethanol metabolism. Ethanol inhibition of drug metabolism in vitro appears to result from a modification of the lipophilic milieu that surrounds the cytochrome P-450 in the microsomal membrane. Interference with the hydrophobic sites may either directly or indirectly affect the catalytic activities of the microsomal enzyme.

Animals↗
PubMed2025

Health-associated key gut microbiota drives the variation in community metabolic interactions in non-human primates.

Gut microbiota often undergo metabolic cross-feeding and resource competition. However, our understanding of global variations in these interactions and their implications for host health remain elusive. By analyzing a microbial genome catalog from 841 fecal metagenomes across 53 primate species worldwide, we identified key microbiota assigned to two taxa, i.e., Bacillota_A and Pseudomonadota, which well predicted the trade-off of community-level interaction types between metabolic competition and cooperation. Specifically, Bacillota_A species were inherently competitive and amino acid auxotrophic and typically found in anaerobic habitats. In contrast, members of Pseudomonadota were inherently cooperative, siderophore producers, and more abundant in aerobic conditions. Random forest models successfully distinguished unhealthy gut samples from healthy samples through the key competitive and cooperative microbiota, suggesting potential links between community metabolic interactions and host health. Together, this study enhances our mechanistic understanding of microbial interaction dynamism within complex gut ecosystems, offering new targets for understanding host health.

Animals↗
PubMed1975

Metabolic interactions of glucose, acetoacetate and adrenaline in rat submaxillary gland in vitro.

1. The metabolic interactions between glucose, acetoacetate and adrenaline were studied in submaxillary-gland slices. 2. Acetoacetate (2.5 mM) inhibited glucose removal by 22% and entry of glucose carbon into the tricarboxylic acid cycle by 54%. 3. Acetoacetate caused an increase in (glucose 6-phosphate) together with an increase in (citrate), a finding that suggests that the phosphofructokinase step might be inhibited by the elevated (citrate). Support for this suggestion was obtained in experiments in which fluoracetate was used to elevate (citrate). 4. A further site of action of acetoacetate at the pyruvate dehydrogenase step was suggested by an increase in the lactate+pyruvate pool, and the finding that pyruvate removal and (3-14C)pyruvate oxidation were inhibited by acetoacetate. 5. Adrenaline, a stimulator of secretion by this tissue, increased glucose removal by 25%. Adrenaline increased glucose removal to the same extent when acetoacetate was also present in the incubation medium. In both cases the increase was accompanied by a fall in (glucose 6-phosphate). 6. Adrenaline also overcame the inhibition of pyruvate removal caused by acetoacetate. 7. The tissue (ATP) decreased by about 50% on addition of adrenaline, and a similar fall was observed in vivo after adrenergic stimulation by isoproterenol. 8. Omission of Ca-2+ from the medium prevented the fall in (glucose 6-phosphate) and (ATP) caused by adrenaline, although adrenaline was still able to stimulate glucose removal. The inhibitory effect of acetoacetate on gluocse removal was reversed by adrenaline, but there was no stimulation above the control rates. Inhibition of pyruvate removal by acetoacetate was not overcome by adrenaline in the absence of Ca-2+. 9. Dibutyryl cyclic AMP had no effect on glucose removal or on (ATP). 10. Possible mechanisms by which adrenaline can bring about its metabolic effects are discussed.

Acetoacetates↗
PubMed1975

Metabolic interactions of dichloroacetate and insulin in experimental diabetic ketoacidosis.

1. The infusion of sodium dichloroacetate into rats with severe diabetic ketoacidosis over 4h caused a 2mM decrease in blood glucose, and small falls in blood lactate and pyruvate concentrations. Similar findings had been reported in normal rats (Blackshear et al., 1974). In contrast there was a marked decrease in blood ketone-body concentration in the diabetic ketoacidotic rats after dichloroacetate treatment. 2. The infusion of insulin alone rapidly decreased blood glucose and ketone bodies, but caused an increase in blood lactate and pyruvate. 3. Dichloroacetate did not affect the response to insulin of blood glucose and ketone bodies, but abolished the increase of lactate and pyruvate seen after insulin infusion. 4. Neither insulin nor dichloroacetate stimulated glucose disappearance after functional hepatectomy, but both agents decreased the accumulation in blood of lactate, pyruvate and alanine. 5. Dichloroacetate inhibited 3-hydroxybutyrate uptake by the extra-splachnic tissues; insulin reversed this effect. Ketone-body production must have decreased, as hepatic ketone-body content was unchanged by dicholoracetate yet blood concentrations decreased. 6. It was concluded that: (a) dichloroacetate had qualitatively similar effects on glucose metabolism in severely ketotic rats to those observed in non-diabetic starved animals; (b) insulin and dichloroacetate both separately and together, decreased the net release of lactate, pyruvate and alanine from the extra-splachnic tissues, possibly through a similar mechanism; (c) insulin reversed the inhibition of 3-hydroxybutyrate uptake caused by dichloroacetate; (d) dichloroacetate inhibited ketone-body production in severe ketoacidosis.

Acetates↗
PubMed1979

Metabolic interaction between amitriptyline and perphenazine in psychiatric patients.

1. Steady-state plasma level samples of sixty-five schizophrenic patients from two psychiatric hospitals assigned to three treatment groups (amitriptyline 150 mg/day, perphenazine 20 mg/day and a combination of amitriptyline and perphenazine at 150 mg and 20 mg/day) were assayed for amitriptyline (AT), endogenous nortriptyline (NT) and perphenazine (PPZ) using gas-liquid chromatography. 2. Results reveal that AT and NT levels are independent of sex and hospital environment. 3. PPZ significantly increased the steady-state NT plasma levels, probably through inhibition of the hydroxylation biotransformation pathway, but had no effect on AT levels, thus indicating that PPZ has no influence on the desmethylation pathway, or alternatively, the hydroxylation of AT.

Adult↗
PubMed1979

Studies on nickel metabolism: interaction with other mineral elements.

Nickel toxicity was studied in young chicks fed a semi-purified diet. Dietary nickel concentrations of 300 mg/kg and higher resulted in significant reduction in growth rate. Mortality and anemia were observed in chicks receiving 1100 mg/kg nickel. Dietary nickel content of 300 mg/kg resulted in a significant increase in kidney nickel content while higher dietary levels were required to affect the nickel content of other body tissues. Supplementation of nickel toxic diets (500 mg/kg) with 100 mg/kg of cobalt, iron, copper, and zinc did not alleviate the symptoms of nickel toxicity or consistently affect tissue nickel accumulation. The addition of cobalt resulted in a further depression in growth rate when added to the nickel toxic diet. However, subsequent studies showed that this was due to the toxicity of cobalt and no evidence was found for an interaction between these two elements. The lack of interaction of nickel with copper, iron, and zinc is in contrast to the results observed by other investigators at low dietary concentrations of nickel.

Animals↗
PubMed1975

[Strontium and calcium metabolism. Interaction of strontium and vitamin D].

Oral administration of strontium to calcium wellfed rats blocks the intestinal absorption of calcium. When high doses of vitamine D are given over long period, the inhibition of calcium intestinal absorption disapears. Under these conditions the absorption of strontium is increased. It is suggested that there is only one absorption mechanism for these two cations. An overdose of the vitamine D increases the renal elimination of strontium but under these conditions the plasma concentration of the strontium is unchanged. Vitamine D brings about the some action on the bone fixation of the strontium as it does on the bone fixation of calcium. The bone fixation is increased with low dosages. The bone fixation is decreased with high dosages.

Animals↗
PubMed1976

[Diphenylhydantoin. Metabolism, pharmacokinetics, interactions and side effects].

The metabolism, mechanism of action, interactions with other drugs and side effects of diphenylhydantoin (DPH), which is probably the most commonly used antiepileptic drug are reviewed in the light of the recent literature. Some findings of practical importance are emphasized, and the resultant implications with regard to the management of epileptic patients are discussed.

Anti-Anxiety Agents↗
PubMed1978

Effects of baclofen on dopamine metabolism and interaction with neuroleptic effects.

Baclofen increased striatal levels of dopamine (DA), homovanillic (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) dose-dependently above 10 mg/kg i.p. The effect on the DA metabolites was shown to be caused only by the (-)-isomer. The HVA increase after 20 mg/kg i.p. was not antagonized by either scopolamine or picrotoxin. Repeated treatment produced a smaller increase in HVA than a single administration. Baclofen reduced both the disappearance of DA after alpha-methyl-p-tyrosine and the acceleration of the DA disappearance caused by neuroleptics in corpus striatum and in the mesolimbic area. The neuroleptic-induced increases in HVA and DOPAC and in DOPA accumulation after central decarboxylase inhibition were also reduced. Picrotoxin could not antagonize these effects of baclofen which therefore cannot be regarded as being garbergic. Baclofen effects on DA metabolism are similar to those reported for gamma-hydroxybutyric acid and are probably a consequence of inhibition of firing of DA neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Platelet and blood vessel arachidonate metabolism and interactions.

Exogenous arachidonate addition to intact platelets, in the absence or the presence of blood vessel microsomes, results in the production of thromboxane B(2) (the stable degradation product of thromboxane A(2)) only. Prostaglandin (PG) endoperoxides are released from intact platelets only when thromboxane synthetase is inhibited. Thus, addition of exogenous arachidonate to imidazole-pretreated platelets in the presence of bovine aorta microsomes (source of prostacyclin synthetase) results predominantly in the synthesis of 6-keto-PGF(1alpha) (the stable degradation product of prostacyclin). Strips of intact aorta were removed from aspirin-treated rabbits, thus the isolated blood vessels were unable to convert endogenous or exogenous arachidonate to prostacyclin. Human platelets, with [(14)C]arachidonate-labeled phospholipids, adhered to the blood vessel segments and released some thromboxane B(2). The subsequent addition of thrombin facilitated the release of endogenous arachidonate and thromboxane, but no labeled 6-keto-PGF(1alpha) was detectable. There is therefore no direct chemical evidence of PG-endoperoxide release from human platelets during either aggregation or adhesion, which therefore precludes the possibility that blood vessels use platelet PG-endoperoxide for prostacyclin synthesis. Imidazole inhibited the thromboxane synthetase in the labeled platelets, and thereafter thrombin stimulation resulted in the release of platelet-derived, labeled PG-endoperoxides that were converted to labeled prostacyclin by the vascular prostacyclin synthetase. The latter result suggests a potential antithrombotic therapeutic benefit might be achieved using an effective thromboxane synthetase inhibitor.

Animals↗
PubMed2026

From isolation to insights: mitochondrial complex I in the diatom Phaeodactylum tricornutum.

Diatoms are among the most ecologically successful microalgae, contributing significantly to marine primary production and global carbon cycling. Their distinctive metabolic architecture, shaped by a complex evolutionary history involving secondary endosymbiosis, includes a highly compartmentalized cell organization and unique metabolic pathways. In Phaeodactylum tricornutum, a model pennate diatom, chloroplasts with four membranes and mitochondria of likely exosymbiotic origin exhibit intricate physical and metabolic interactions that support integrated carbon and nitrogen metabolism. The mitochondrial electron transport chain, essential for ATP synthesis, shows clade-specific structural and compositional adaptations. Despite its importance, detailed proteomic characterization has remained limited. Here, we report a method for the isolation of mitochondrial complex I from P. tricornutum and present a comprehensive proteomic analysis. Our results confirm the presence of carbonic anhydrase and bridge modules, both previously proposed as ancestral features of mitochondrial complex I, and identify at least one novel, clade-specific subunit that resembles NAD(P)H-dependent trans-2-enoyl-CoA/ACP reductases (TER) from other species. The subunit is similar to proteins involved in mitochondrial fatty acid biosynthesis. Our findings provide new insights into the composition, evolutionary conservation, and potential biotechnological relevance of this essential respiratory protein complex in diatoms.

Diatoms↗