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Results for “AMINO ACID METABOLISM”

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At least 487 records · Page 27Linked to original sources
PubMed1985

Effect of clofibrate on branched-chain amino acid metabolism.

Clofibric acid inhibited the oxidative decarboxylation of 4-methyl-2-oxopentanoate and 3-methyl-2-oxobutanoate in mitochondria and homogenates of rat liver and quadriceps muscle. In rat hemidiaphragms clofibric acid inhibited the oxidative decarboxylation of 4-methyl-2-oxopentanoate and had no effect on that of 3-methyl-2-oxobutanoate. Clofibric acid displaced branched-chain 2-oxo acids from bovine serum albumin. Clofibrate-treatment of rats decreased the actual activity and activity state of the branched-chain 2-oxo acid dehydrogenase complex in quadriceps muscle, and increased the total activity in heart and liver without a change of the activity state. All interactions of clofibric acid with the metabolism of branched-chain amino acids appear to relate to its structural resemblance to the branched-chain 2-oxo acids. Both reduced plasma and muscle concentrations of branched-chain amino acids and reduced muscle oxidation may play a role in the myopathic side-effects of clofibrate-treatment.

2-Oxoisovalerate Dehydrogenase (Acylating)↗
PubMed1990

High-performance liquid chromatographic analysis of alpha-keto acids produced from amino acid metabolism in oral Bacteroides.

Profiles of metabolic alpha-keto acids were determined by a high-performance liquid chromatographic method and applied to characterization of oral black-pigmented Bacteroides. Each bacterial strain was incubated with amino acids in a chemically defined medium. After production alpha-keto acids were purified by hydrazide gel column treatment and converted to u.v.-absorbing derivatives. They were analysed by reversed-phase ion-pair chromatography. Black-pigmented Bacteroides species were differentiated into two groups according to production of aromatic alpha-keto acids. Bacteroides gingivalis, B. endodontalis and B. loescheii produced both p-hydroxyphenylpyruvic and phenylpyruvic acids. However, no such alpha-keto acids were produced by B. levii, B. intermedius and B. denticola. In addition, production profiles of several aliphatic alpha-keto acids (alpha-ketoglutaric, pyruvic, alpha-ketobutyric, alpha-ketoisovaleric, alpha-ketoisocaproic, and alpha-keto-beta-methylvaleric acids) separated each individual species in such groups. The present study offers useful chemotaxonomic information on amino acid metabolic activity of oral black-pigmented Bacteroides species.

Amino Acids↗
PubMed2004

Ammonium exposure and pyruvate affect the amino acid metabolism of bovine blastocysts in vitro.

The accumulation of ammonium is a major artefact of in vitro embryo culture. This study has examined ammonium production and potential mechanisms of disposal in preimplantation bovine blastocysts. Embryos were produced by in vitro maturation and fertilisation of oocytes, and cultured in synthetic oviduct fluid containing amino acids and BSA (SOFaaBSA). Ammonium/urea concentrations were determined enzymatically. Amino acid appearance/disappearance 'profiles' of single blastocysts were determined at 0, 1.25 and 2.5 mM NH(4)Cl (with or without 0.33 mM pyruvate), and with or without 10 mM dipicolinic acid (DPCA; a glutamate dehydrogenase (GLDH) inhibitor) or 2 mM amino-oxyacetate (AOA; a transaminase inhibitor). Free ammonium was produced at a rate of 4.281 (+/-0.362) pmol/embryo/h, while urea production was undetectable. The presence/absence of pyruvate affected amino acid profiles, especially alanine appearance (P < 0.001), glutamate disappearance (P < 0.05) and overall turnover (the sum of appearance and disappearance) (P < 0.001). GLDH inhibition with DPCA had no effect on amino acid overall disappearance, but glutamate disappearance increased, while that of arginine decreased (P < 0.05). The transaminase inhibitor, AOA, depressed turnover (P < 0.05), aspartate and glutamate disappearance, and alanine appearance. Thus, bovine blastocysts release ammonium as free ions or fix them, not as urea, but as alanine, possibly glutamine and, less likely, arginine. An active role for GLDH and transaminases in regulating blastocyst amino acid metabolism was demonstrated.

Alanine↗
PubMed1977

Isolation and identification of aliphatic short-chain acylcarnitines from beef heart: possible role for carnitine in branched-chain amino acid metabolism.

Aliphatic acylearnitines isolated from a water-soluble fraction of beef heart have been characterized by gas chromatography and mass spectrometry. The following acyl residues derived from the acylcarnitine fraction were unequivocally identified: acetyl, propionyl, isobutyryl, butyryl, alpha-methylbutyryl, valeryl, isovaleryl, tiglyl, and caproyl. beta-methylcrotonyl and methacrylyl were tentatively identified. This occurrence of considerable quantities of branched-chain acylcarnitines indicates a role for carnitine in branched-chain amino acid metabolism.

Amino Acids↗
PubMed1990

Studies of myocardial protection in the immature heart. II. Evidence for importance of amino acid metabolism in tolerance to ischemia.

This study tests the importance of amino acid transamination in determining the tolerance of immature hearts to ischemic damage. Amino acid transamination was inhibited metabolically by pretreatment with aminooxyacetic acid. The aminooxyacetic acid dose and duration were determined by incubating in vitro tissue homogenate and showing that an 8 mmol/L AOA dose for 5 minutes blocked 90% of alanine aminotransferase and aspartate aminotransferase activity. Control studies in nonischemic hearts showed that coronary perfusion with aminooxyacetic acid for 5 minutes did not impair myocardial performance. In contrast, pretreatment of immature puppies with aminooxyacetic acid severely impaired recovery after 45 minutes of normothermic global ischemia (30% versus 85% recovery in untreated hearts, p less than 0.05). Biochemical analyses of hearts undergoing ischemia showed aminooxyacetic acid to limit lactate production, impair glutamate utilization, prevent alanine production, and limit succinate accumulation (p less than 0.05). These data suggest that amino acid transamination is an important adaptive process in the immature heart that improves its resistance to ischemic damage.

Adenosine Triphosphate↗
PubMed2003

Altered amino acid metabolism in chronic obstructive pulmonary disease: new therapeutic perspective?

PURPOSE OF REVIEW: Wasting of muscle mass, commonly present in patients with chronic obstructive pulmonary disease, is a complex process involving changes in the control of intermediary metabolism as well as in muscle cell status. Although research exploring intermediary metabolism in chronic obstructive pulmonary disease is still in its infancy, there is an increased interest in a potential role for amino acids in modulating muscle anabolism. This review aims at summarizing and critically evaluating the available clinical studies examining alterations in amino acid profile in plasma and skeletal muscle of patients with chronic obstructive pulmonary disease. RECENT FINDINGS: All studies show pronounced alterations in plasma and muscle amino acid status in patients with chronic obstructive pulmonary disease but no consistent "disease specific" pattern for most amino acids. Variability is likely influenced by the heterogeneity of the disease with respect to lung function and nutritional state. Nevertheless, general consistency exists in chronic obstructive pulmonary disease with respect to (1) a reduced plasma branched-chain amino acid level, and (2) a decreased muscle glutamate concentration. Alterations in branched-chain amino acid metabolism appear to be influenced by the degree of muscle wasting, while the reduction in muscle glutamate is related to the diffusing capacity as a hallmark of emphysema. The reduction in glutamate status is associated with reduced muscle glutathione levels and appears to be linked to enhanced glycolysis as evidenced from an accelerated increase in plasma lactate during exercise. SUMMARY: Underlying mechanisms of the observed alterations in amino acid profile in chronic obstructive pulmonary disease, and the influences of disease associated mediators such as chronic low-grade inflammation and (chronic and intermittent) hypoxia are speculative and need to be explored in experimental study designs.

Amino Acids↗
PubMed1995

Altered tissue amino acid metabolism in acute T-2 toxicosis.

T-2 toxin is a Fusarium trichothecene mycotoxin that has been shown to alter brain neurochemistry and eating behavior in animals eating contaminated diets. Experiments were conducted to determine the role of altered tissue amino acid metabolism in the etiology of acute T-2 toxicosis. Fasted weanling rats were orally dosed with 0 or 2.0 mg T-2 toxin/kg body weight. Blood, brain, liver, and muscle tissue were excised 4 and 8 hr after dosing, and amino acid concentrations were determined. Hepatic enlargement coupled with reduced liver concentrations of free small neutral, large neutral, and basic amino acids were seen 4 hr after dosing. Brain and muscle amino acid concentrations were largely refractory to treatment, while the plasma concentrations of tyrosine and lysine, and the sum of the basic amino acids fell. Hepatic amino acid concentrations returned to control levels 8 hr after dosing at which time aminoacidemia was seen. This was due partially to an increase in plasma concentrations of large neutral amino acids including particularly the branched-chain amino acids. A subsequent experiment was conducted to determine the effect of T-2 toxin on 14C-leucine uptake and incorporation into protein in liver slices 4 hr after dosing. Exposure to T-2 toxin reduced total (free + protein-bound) uptake of leucine due primarily to reduced incorporation of leucine into newly-synthesized hepatic protein. It was concluded that reduced amino acid uptake by liver preceded aminoacidemia in acute T-2 toxicosis, although it is not clear how this might influence subsequent changes in brain neurochemistry and behavior.

Amino Acids↗
PubMed1999

Hepatic injury and disturbed amino acid metabolism in mice following prolonged exposure to organophosphorus pesticides.

Chronic occupational exposure to organophosphorus and carbamate-type pesticides significantly inhibits acetylcholinesterase activity and causes morbidity. This study on mice was designed to evaluate their amino profile and to identify signs of hepatic dysfunction following their chronic exposure to mixtures of organophosphorus pesticides. Laboratory mice were exposed to a formulated mixture of the six organophosphorus pesticides (Dimethoate, Chlorpyrifos, Profenofos, Pirimiphos methyl, Triazophos and Dimethoate) most commonly used in agriculture in this region of the Middle East. Doses (10% of LD50 of the mixture) were given once a week by gavage in corn oil for 7 weeks; the control group was given only corn oil. At the end of the exposure period, mice were culled and blood samples were collected to determine erythrocyte acetylcholinesterase activity, biochemical markers of liver function and concentrations of serum amino acids. Erythrocyte acetylcholinesterase activity and total serum proteins decreased significantly in the exposed group. Serum concentrations of alanine aminotransferase and aspartate aminotransferase, alanine, glutamic acid, glycine, isoleucine, leucine, methionine, ornithine, proline, serine, threonine and valine were significantly increased in the exposed mice, while serum levels of cystine were decreased significantly. There were also non-significant increases in serum alkaline phosphatase, gama-glutamyl transpeptidase and some of the other amino acids. Chronic exposure to mixtures of organophosphorus pesticides is associated with decreased acetylcholinesterase activity, hepatic dysfunction and disturbance of amino acids profile. Biochemical indices of hepatocellular injury and disturbed amino acid metabolism may be of value as markers of chronic exposure to such pesticides.

Acetylcholinesterase↗
PubMed1986

Amino acid metabolism after lambda-carrageenan injury to rat skeletal muscle.

To evaluate whether the alterations in amino acid (AA) metabolism that follow the lambda-carrageenan injury are direct consequences of wounding and are therefore independent of food intake, plasma AA, in vivo muscle intracellular free AA, and AA release during isolated hindlimb perfusions were determined in pentobarbital-anesthetized rats with lambda-carrageenan-induced hindlimb muscle wounds (W) and in pair-fed (PFC) and ad libitum-fed (ALC) non-wounded controls. Both PFC and W animals showed different plasma and muscle intracellular AA composition that ALC. The alterations observed in these compartments in W animals may not have resulted exclusively as a consequence of the wound. Wounded hindlimbs released more AA during perfusion than either control group. The marked increase in net protein catabolism of W muscle appeared to be related to wounding and not a consequence of partial starvation. The normalized release (amino acid/phenylalanine ratio) of glutamine (W less than ALC), alanine (W less than PFC and ALC), and the branched-chain amino acids (W greater than PFC and ALC) differed among groups, suggesting an alteration in the metabolism of these AA in W tissue.

Alanine↗