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At least 631 records · Page 35Linked to original sources
PubMed1988

Labeling of porphobilinogen deaminase by radioactive 5-aminolevulinic acid in isolated developing pea chloroplasts.

A protein had been previously described, which was labeled by radioactive 5-aminolevulinic acid in isolated developing chloroplasts. In the present study we have shown that this protein (Mr approximately equal to 43,000) probably exists as a monomer in the chloroplast stroma. The labeling is blocked if known inhibitors of 5-aminolevulinic acid dehydratase are added to the incubation mixture, and is markedly decreased in intensity if nonradioactive 5-aminolevulinate or porphobilinogen are added to the incubation mixture; other intermediates in the porphyrin biosynthetic pathway, uroporphyrinogen III, uroporphyrin III, and protoporphyrin IX, do not decrease the labeling of the 43-kDa protein appreciably. Nondenaturing gels of the proteins isolated from the incubation with radioactive 5-aminolevulinic acid were stained for porphobilinogen deaminase activity. A series of red fluorescent bands was obtained which coincided with the radioactive bands visualized by autoradiography. It is concluded that the soluble chloroplast protein that is labeled in organello by radioactive 5-aminolevulinic acid is porphobilinogen deaminase.

Aminolevulinic Acid↗
PubMed1993

Formation of platelet-activating factor-like phospholipids by Fe2+/ascorbate/EDTA-induced lipid peroxidation.

We have identified novel phospholipids together with platelet-activating factor and its 1-acyl analogues in purified fractions from a bovine brain lipid extract. These novel compounds were phospholipids with an sn-2-short-chain monocarboxylyl, dicarboxylyl or omega-hydroxymonocarboxylyl group. The profiles of these three types of phospholipids suggest that they were formed by lipid peroxidation. To examine this possibility, we peroxidized synthetic phosphatidylcholines (PC) with an sn-2-polyunsaturated fatty acyl group and PC from bovine brain, with Fe2+/ascorbate/EDTA, and analyzed the secondary degradation products retaining a glycerol backbone by fast atom bombardment-mass spectrometry and GC-MS. Results showed the formation of four kinds of PC with a short-chain monocarboxylate, dicarboxylate, dicarboxylate semialdehyde or omega-hydroxymonocarboxylate moiety. The chain lengths of these PC were related to the position of the double bond vicinal to the esterified carbonyl group in the sn-2-long-chain acyl moiety of the parent PC. The molecular heterogeneity of secondary products formed by the oxidative degradation of bovine brain PC resembled those of the unique phospholipids that we previously detected in the fractions with platelet-activating factor-like activity purified from a bovine brain lipid extract, although the former lacked the species with an acetyl group. These results suggest that all the novel phospholipids with a short-chain acyl group in the brain lipid extract except that with an acetyl group were produced by lipid peroxidation.

Animals↗
PubMed1987

Nonenzymatic synthesis of delta-aminolevulinate (ALA) by cobalt (Co++).

Cobalt, a metal known to modulate the heme biosynthetic enzymes, is shown to be capable of catalysing the formation of ALA through a transamination reaction. The transamination reaction follows a double-displacement reaction kinetics. Further, it has also been shown that the product of the reaction catalysed by cobalt can be used by the enzyme ALA dehydratase as the substrate in the formation of porphobilinogen. The formation of ALA by cobalt can be inhibited by the intermediates of the heme biosynthetic pathway, mainly protoporphyrin. Heme, on the other hand, does not have any effect on the reaction at all concentrations tested.

Alanine↗
PubMed1984

Neuropharmacology of delta-aminolaevulinic acid--I. Effect of acute administration in rodents.

Delta-aminolaevulinic acid (ALA) is suspected of being responsible for the neuropsychiatric symptoms of acute porphyria. The object of this study was to examine the effects of ALA in vivo on a range of behavioural and physiological functions which are known to be affected in the acute porphyric attack. Aminolaevulinic acid was administered by intraperitoneal or subcutaneous injection to mice in doses up to 1000 mg/kg and effects on nociception (hot-plate and abdominal constriction tests), CNS excitability (pentobarbitone sleep-time and pentylenetetrazole-induced seizures), motor co-ordination and grip (rotating rod test) were studied. Rats were given intravenous injections or infusions of ALA of up to 24 mg and changes in blood pressure, heart rate and ED50 for noradrenaline, acetylcholine and isoprenaline examined. No statistically significant effects were noted, using buffered solutions of ALA (pH 7.0-7.4). However, unbuffered solutions of ALA caused significant bradycardia and hypotension. These results do not support the hypothesis that ALA has significant acute neuropharmacological activity in vivo when the blood-brain barrier is intact.

Aminolevulinic Acid↗
PubMed1978

Delta-aminolaevulinic acid metabolism in normal and lead-exposed humans.

The activity of the haem biosynthetic enzymes delta-aminolaevulinic acid synthetase (ALA.S) and delta-aminolaevulinic acid dehydratase (ALA.D) were measured in the peripheral blood of a group of lead workers and control subjects. The haem precursor delta-aminolaevulinic acid (ALA) was measured in blood and urine, whilst lead levels were measured in whole blood. The inter-relationships between all these parameters were examined and quantified. The results demonstrate that above a blood lead concentration of 2 mumole/l and below an erythrocyte ALA.D activity of 18 nmole ALA utlized/min/ml red blood cells (R.B.C.), Haem synthesis is depressed to such an extent that the activity of leucocyte ALA.S, the rate-limiting enzyme of haem biosynthesis, is increased by negative feedback.

5-Aminolevulinate Synthetase↗
PubMed1984

Neuropharmacology of delta-aminolaevulinic acid. II. Effect of chronic administration in mice.

delta-Aminolaevulinic acid (ALA) is suspected of being responsible for the neuropsychiatric symptoms of acute porphyria. The object of this study was to examine the effects of continuous administration of ALA in vivo on behaviour known to be affected in acute porphyria. ALA was administered to mice via minipumps implanted subcutaneously. Mean urinary excretion of ALA over the ensuing 7 days was approximately 80 mumol/kg b. wt./day. No significant effects on locomotor activity, motor co-ordination and grip and noci-perception were noted. These results do not support the hypothesis that chronic exposure of animals to ALA may produce a porphyria-like syndrome.

Aminolevulinic Acid↗
PubMed1989

delta-Aminolevulinic acid biosynthesis in Escherichia coli and Bacillus subtilis involves formation of glutamyl-tRNA.

Cell-free extracts of Escherichia coli and Bacillus subtilis catalyzed the tRNA-dependent, RNase A-sensitive formation of delta-aminolevulinic acid (ALA) from glutamate. Cell extracts prepared from cultures of E. coli grown under aerobic or anaerobic conditions had similar levels of ALA biosynthetic activity. Both the tRNA-stimulated conversion of glutamate to ALA and the conversion of glutamate-1-semialdehyde to ALA were inhibited by gabaculin. However, gabaculin had no effect on the growth of either E. coli or B. subtilis. The tRNA-dependent transformation of glutamate to ALA in E. coli and B. subtilis thus appears to be very similar to the pathway found in cyanobacteria, certain obligate anaerobic eubacteria, archaebacteria and in the chloroplasts of algae and higher plant species.

Alanine↗
PubMed1979

Determination of 5-aminolaevulinic acid and porphobilinogen by high-performance liquid chromatography.

A strong anion-exchange column coupled to a strong cation-exchange column with acetate buffer as eluent or reversed-phase ion-pair chromatography on octadecylsilica with methanol-water containing 1-heptanesulphonic acid as the mobile phase is described for the simultaneous separation of 5-aminolaevulinic acid and porphobilinogen. The separation is applied to the development of a fast and simple method for determining the activity of the enzyme aminolaevulinic acid dehydrase in human erythrocytes. 5-Aminolaevulinic acid is used as the enzyme substrate and the enzyme activity is expressed as micromoles of porphobilinogen formed per ml of erythrocytes in 1 h at 38 degrees. 5-Aminolaevulinic acid and porphobilinogen can also be separated from the urine of prophyric patients but the UV detector has insufficient sensitivity for the determination of 5-aminolaevulinic acid.

Aminolevulinic Acid↗
PubMed1977

Tyrosinemia with acute intermittent porphyria: aminolevulinic acid dehydratase deficiency related to elevated urinary aminolevulinic acid levels.

A patient who had hereditary tyrosinemia was observed during two illnesses to have characteristics of acute intermittent porphyria with associated hypertension. Metabolic studies revealed elevated levels of urinary aminolevulinic acid but normal levels of porphyrin metabolites associated with, and possibly explained by, decreased red blood cell activity of the zinc-dependent enzyme, aminolevulinic acid dehydratase. Zinc deficiency could not be directly associated with the diminished enzyme activity. The patient's hypertension appeared to be related to increased urinary excretion of catecholamines and to elevated renin activity in peripheral venous blood.

Adolescent↗
PubMed1988

5'-Levulinyl and 2'-tetrahydrofuranyl protection for the synthesis of oligoribonucleotides by the phosphoramidite approach.

The levulinyl group has been employed for protection of the 5'-hydroxyl group in the synthesis of oligoribonucleotides by the phosphoramidite approach, using the acid-labile 2'-tetrahydro-furanyl group. The hydrazine treatment was performed for 10 minutes in order to remove the levulinyl group on controlled pore glass. Four decaribonucleotides (AAAAAAAAAU, GGGGGGGGGU, CCCCCCCCCU and UUUUUUUUUU) and a heneicosamer (GCCUAGCUGAUGAAGGGUGAU) were prepared with an automatic synthesizer in good yields.

Aminolevulinic Acid↗
PubMed1976

Quantitation of ineffective erythropoiesis from the incorporation of [15N] delta-aminolaevulinic acid and [15N] glycine into early labelled bilirubin. I. Normal subjects.

The incorporation of [15N] glycine into early labelled bilirubin and haemoglobin haem was measured in four haematologically normal subjects, using the clearance of [14C] bilirubin to measure total bilirubin production rate. Hepatic haem turnover was calculated from the incorporation of [15N]=sigma-aminolaevulinic acid into early labelled bilirubin. From the exprimental data previously published data in normal subjects a method is derived for the quantitation of ineffective erythropoiesis which can be applied to similar studies in patients with haematological disorders.

Aged↗