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Results for “LEVULINIC ACID”

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PubMedDate not supplied

Effect of lead on erythropoietic system of intact and splenectomized rats.

Erythropoietic alterations in normal and splenectomized mature male rats treated with aqueous lead acetate intraperitoneally at dosages of 4 mg/kg and 6 mg/kg body weight were observed over a period of 30 days. Significant retardation in growth might be due to gradual increases in lead toxicity. The elevated blood lead level, increased urinary delta-amino-levulinic acid (ALA-U) excretion, depletion in RBC and haemoglobin content and more number of reticulocytes in peripheral blood indicated the increased intensity of lead toxicity and inhibitory effect on haem biosynthesis. The accelerating action of lead on erythropoietic cellular series i.e. pronormoblast, early and intermediate normoblast and late normoblast was evident by the significant increase in number of cellular count both in intact and splenectomized rats after treatment with lead.

Animals↗
PubMed1981

[Mechanism of delta-aminolevulinic acid neurotoxicity].

The neurotoxicity of delta-aminolaevulinic acid (ALA), porphobilinogen (PBG), glutamic acid, gamma-aminobutyric acid and kainic acid was compared in order to investigate the possibility of a common neurotoxic mechanism. Only ALA (10 microM) and glutamic acid (1 mM) were toxic towards neurons in culture, as measured by cell survival after 5 days' exposure. 3H-kainic acid binds to striatal membranes with an equilibrium dissociation constant (KD) of 57 nM and the number of binding sites was found to be 20 pmol/g striatal tissue. However, neither of the porphyrin precursors could displace kainic acid from these binding sites. Kainic acid alone caused neuronal degeneration after intrastriatal administration, as determined by 3H-spiroperidol binding to striatal membranes. The porphyrin precursors ALA and PBG thus do not share a common neurotoxic mechanism with the well-known neurotoxin kainic acid.

Aminolevulinic Acid↗
PubMedDate not supplied

Depression of the hepatic cytochrome P-450 mono-oxygenase system by administered tilorone (2,7-bis(2-(diethylamino)ethoxy)fluoren-9-one dihydrochloride).

The oral administration of the antiviral agent, tilorone-HCl (50 mg/day for 4 days) to rats caused losses of hepatic microsomal ethylmorphine N-demethylase, benzo(a)pyrene hydroxylase and aniline hydroxylase activities of 50, 44 and 22%, respectively. Microsomal levels of cytochrome P-450 and NADPH-cytochrome c reductase were lowered by 40 and 20% respectively, but levels of cytochrome b5 and NADH-cytochrome c reductase remained unchanged. After a single oral dose of tilorone-HCl (50 mg/kg) a loss of 38% of the microsomal cytochrome P-450 and 25% of the ethylmorphine N-demethylase activity was observed within 24 hr; recovery was complete within 8 to 10 days. Hexobarbital sleeping times and blood levels were elevated after tilorone administration (20 or 50 mg/kg/day for 4 days). In vitro, tilorone-HCl showed no inhibitory effect on microsomal drug metabolism nod did it affect the cytochrome P-450 content of the microsomes. The rate of incorporation of delta-amino(3H)levulinic acid into cytochrome P-450 was not affected by tilorone-HCl.

Aniline Hydroxylase↗
PubMed1984

Regulation of light-harvesting chlorophyll-binding protein mRNA accumulation in Chlamydomonas reinhardi. Possible involvement of chlorophyll synthesis precursors.

Light induction of light-harvesting chlorophyll a/b-binding protein (LHCP) mRNA accumulation was studied in light-dark synchronized cultures of Chlamydomonas reinhardi. LHCP mRNA accumulation was prevented by the chlorophyll-synthesis inhibitor alpha,alpha-dipyridyl which blocks late steps in the chlorophyll biosynthetic pathway and leads to the accumulation of the porphyrin intermediate magnesium protoporphyrin methyl ester. LHCP mRNA accumulated normally, however, when chlorophyll synthesis was blocked by inhibitors such as hemin and levulinic acid which interfere with early steps in the chlorophyll biosynthesis pathway prior to the formation of magnesium protoporphyrin methyl ester. Similar effects were observed in the light induction of LHCP mRNA levels in protoporphyrin IX-accumulating mutants, brc-1 and brs-1. These mutants have low levels of LHCP mRNA when grown under heterotrophic conditions in the dark where they accumulate protoporphyrin IX. However, LHCP mRNA is light-induced in brc-1 which synthesizes chlorophyll in the light and presumably consumes porphyrin intermediates in doing so. These results suggest that the chlorophyll-synthesis intermediates, magnesium protoporphyrin methyl ester and its immediate precursors, inhibit by a feedback mechanism the light induction of LHCP mRNA accumulation. Low magnesium protoporphyrin methyl ester levels permit the light-induced accumulation of LHCP mRNA, whereas high magnesium protoporphyrin methyl ester levels destabilize LHCP mRNA regardless of the illumination conditions. Preliminary experiments show that LHCP mRNA accumulation in C. reinhardi is stimulated by blue light, and not by red light which stimulates LHCP mRNA accumulation in higher plants.

2,2'-Dipyridyl↗
PubMedDate not supplied

[Diabetes mellitus and the biosynthesis of porphyrins].

The blood and urine porphyrin content and porphyrin biosynthesis in the red blood cells after delta-amino levulinic acid (ALA) incubation, porphobilinogen and non-consumed ALA levels, porphobilinogen-synthetase activity were studied in 86 patients divided into 3 groups depending on diabetes severity. Porphyrin separation was investigated by means of thin-layer chromatography. It was found that porphyrin biosynthesis decreases in all diabetics at the early periods of the disease, not depending on its severity. Porphyrin biosynthesis is lowered during a phase of chronic renal insufficiency in patients with diabetic nephropathy. Porphyrin metabolic disorder is caused by hepatic dysfunction and diabetic nephropathy development.

Adult↗
PubMed1983

[Modifications in blood zinc and lead concentrations and ALA-dehydratase activity in optic neuropathy from alcohol and tobacco abuse].

Plasma red blood cell and total blood zinc levels were significantly decreased in 52 consecutives cases of bilateral, retrobulbar, axial optic neuropathy caused by chronic abuse of ordinary wine and/or beer and/or hard beverages and cigarette smoking principally in men in their forties [plasma zinc: 746 mg/l +/- 179 (n = 52), control 907 mg/l +/- 127; red blood cell zinc: 10,218 mg/l +/- 1,327 (n = 10), control 12,244 mg/l +/- 1,307; total blood zinc: 4,849 mg/l +/- 1,069 (n = 51), control 5,831 mg/l +/- 644]. In contrast, blood lead levels were increased in these cases - blood lead: 344 mg/l +/- 101 (n = 30), control 193 mg/l +/- 94. Activity of red blood cell delta-amino-levulinic acid dehydratase (ALA-dehydratase), a zinc dependent enzyme, was decreased [red blood cell ALA-dehydratase; 18,8 IU/l +/- 2,2 (n = 13), control 44,8 IU/l +/- 3,3]. Plasma magnesium was slightly decreased while serum copper was not significantly modified. Possible ophthalmological implication of these findings are discussed.

Alcoholism↗
PubMed1980

[Comparative metabolic studies on [14C]-labelled acemetacin and indometacin in rats (author's transl)].

1. [14C]-Indometacin and [14C]-Acemetacin are synthesized starting from carboxyl-[14C]-levulinic acid. 2. Renal, biliary and fecal elimination of both compounds occurs mainly within 24 h after intravenous or intraduodenal application to rats and after degradation to N-des-p-chlorobenzoyl- and O-des-methyl compounds and various conjugations. Main metabolite in urine and feces after both compounds is O-desmethyl-indometacin. A high percentage of unchanged indometacin besides small amounts of des-p-chlorobenzoylindometacin (DBI) and des-p-chlorobenzoyl-O-desmethylindometacin (DBMI) are found in bile. Both metabolites exist also in urine, bile and feces following administration of acemetacin. 3. After application of [1-(p-chlorobenzoyl)-5-methoxy-2-methylindole-3-acetoxy]-acetic acid (acemetacin, TV 1322, Rantudil) free acemetacin is found to be 2.4% in urine, 7% in the bile and 3.5% in feces. In urine and bile additional amounts are present as conjugates. 4. Conjugation to sulfuric acid was found besides glucuronidation, i.e., O-desmethylindometacinsulfate (urine, bile) and des-p-chlorobenzoyl-O-desmethylindometacinsulfate (bile). indometacin glycine, a new conjugate, is formed after application of either acemetacin or indometacin. The renal proportion of this metabolite is three times higher after acemetacin than after indometacin, this can explain the better tolerance of acemetacin in comparison to indometacin. 5. metabolism of acemetacin and indometacin in the rat, as manifested by excretion into urine, bile and feces, is comparable on a qualitative basis if excretion of free acemetacin is neglected; there exist, however, quantitative differences.

Animals↗
PubMed1981

Formation and disposition of newly synthesized heme in adult rat hepatocytes in primary culture.

Studies with the intact liver have suggested that newly synthesized heme exists transiently in a small pool before its incorporation into tissue heme proteins. The same or a closely related pool may regulate synthesis of heme and serve as the precursor of "early peak" bilirubin. To delineate this postulated pool by a direct approach, we have utilized primary cultures of adult rat hepatocytes. Cultures pulse-labeled with delta-amino[3H]levulinic acid at various time points were fractionated into 105,000 X g supernatant and pellet. Labeled heme appeared within 1 to 2 min in the cytosol fraction, followed by transfer to the pellet. The kinetics of heme formation and transfer and of labeled bilirubin production were analyzed by computer simulation utilizing the least squares method. The experimental findings conformed best to a four-compartment model that includes a second cytosolic heme compartment exchanging with the initially labeled compartment but not serving as a direct precursor of bilirubin. Calculation of apparent rate coefficients indicated that, in cultured hepatocytes, 20% of newly formed heme is converted directly to bile pigment, whereas 80% is utilized for formation of cellular heme proteins (64% in the pellet, 16% in the second cytosol compartment). This experimental approach has provided direct evidence for a rapidly formed cytosolic heme fraction which appears to be identical with the previously postulated regulatory or "unassigned" heme pool of the liver.

Aminolevulinic Acid↗