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Aminolevulinate dehydratase

Porphobilinogen Synthase, delta-aminolevulinic acid dehydratase, ALAD
The ALAD enzyme is composed of 8 identical subunits and catalyzes the condensation of 2 molecules of delta-aminolevulinate to form porphobilinogen (a precursor of heme, cytochromes and other hemoproteins). ALAD catalyzes the second step in the porphyrin and heme biosynthetic pathway; zinc is essential for enzymatic activity. ALAD enzymatic activity is inhibited by lead and a defect in the ALAD structural gene can cause increased sensitivity to lead poisoning and acute hepatic porphyria. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, HAD, CAN, AGE, catalase
Papers on Porphobilinogen Synthase
Influence of abatement of lead exposure in Croatia on blood lead and ALAD activity.
Jasna et al., Zagreb, Croatia. In Environ Sci Pollut Res Int, Jan 2016
We evaluated the effect of lead (Pb) abatement measures in Croatia on blood lead (BPb) concentrations, and delta-aminolevulinic acid dehydratase (ALAD) activity in blood, as a sensitive indicator of early Pb effect.
Association between delta-aminolevulinic acid dehydratase polymorphism and placental lead levels.
Söylemezoğlu et al., Ankara, Turkey. In Environ Toxicol Pharmacol, Jan 2016
UNASSIGNED: Lead inhibits the delta-aminolevulinic acid dehydratase (ALAD) activity and results in neurotoxic aminolevulinic acid accumulation in the blood.
Association between δ-aminolevulinate dehydratase G177C polymorphism and blood lead levels in brain tumor patients.
Abd Elazem et al., Az Zaqāzīq, Egypt. In Mol Clin Oncol, Sep 2015
UNASSIGNED: As the δ-aminolevulinic acid dehydratase (ALAD) G177C polymorphism affects the toxicokinetics of lead in the body, and the corresponding exposure to lead may increase the risk of adult brain tumors, we hypothesize that there is a possible association of the ALAD G177C genotype and the risk of brain tumors in human.
[Study on relationships between biomarkers in workers with low-level occupational lead exposure].
Zhou et al., In Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi, Jun 2015
The blood samples of 233 workers with occupational lead exposure and 76 non-occupational lead exposure were collected to measure the blood lead (Pb-B) level using graphite furnace atomic absorption spectrometry (GFAAS), the zinc Protoporphyrin (ZPP) level with blood fluorescence assay, and the delta-aminolevulinic acid dehydratase (ALAD) concentration by a spectrophotometer, and to determine the gene polymorphism of ALAD with TaqMan real-time polymerase chain reaction.
Relationship among maternal blood lead, ALAD gene polymorphism and neonatal neurobehavioral development.
Qin et al., Xinxiang, China. In Int J Clin Exp Pathol, 2014
ALAD gene polymorphism is associated with lead neurotoxicity.
No ALAD Polymorphism in Bank Vole Populations from Unpolluted and Lead-Zinc Polluted Areas in Poland.
Świergosz--Kowalewska et al., In Folia Biol (krakow), 2014
ALAD (delta aminolevulinic acid dehydratase) gene polymorphism found in human populations results in the existence of two alleles: ALAD1 and ALAD2.
Effects of Lead Exposure and Genetic Polymorphisms on ALAD and GPx Activities in Brazilian Battery Workers.
Barbosa et al., Ribeirão Preto, Brazil. In J Toxicol Environ Health A, 2014
Exposure to the metal may modify the redox status of the cells and consequently result in changes in activities of important enzymes such as delta-aminolevulinic acid dehydratase (ALAD) and glutathione peroxidase (GPx).
Drugs and acute porphyrias: reasons for a hazardous relationship.
Ventura et al., Reggio nell'Emilia, Italy. In Postgrad Med, 2014
In the acute porphyrias (acute intermittent porphyria, hereditary coproporphyria, variegate porphyria, and the very rare delta-aminolevulinic acid dehydratase ALAD-d porphyria), the characteristic severe neurovisceral involvement is mainly ascribed to a tissue accumulation of delta-aminolevulinic acid, a neurotoxic nonporphyrin precursor.
Genotyping an ALAD polymorphism with real-time PCR in two populations from the Iberian Peninsula.
Teixeira et al., Porto, Portugal. In Biochem Genet, 2012
distribution of a single nucleotide polymorphism in two populations from the Iberian Peninsula
Allostery and the dynamic oligomerization of porphobilinogen synthase.
Lawrence et al., Philadelphia, United States. In Arch Biochem Biophys, 2012
The structural basis for allosteric regulation of porphobilinogen synthase (PBGS) is modulation of a quaternary structure equilibrium between octamer and hexamer (via dimers), which is represented schematically as 8mer ⇔ 2mer ⇔ 2mer∗⇔ 6mer∗.
Modification by the genes ALAD and VDR of lead-induced cognitive effects in children.
Pawlas et al., Sosnowiec, Poland. In Neurotoxicology, 2012
This study demonostrated that modification by the genes ALAD lead-induced cognitive effects in children.
Delta-aminolevulinic dehydratase is a proteasome interacting protein.
French et al., Torrance, United States. In Exp Mol Pathol, 2011
The data supports the hypothesis that ALAD, an important enzyme for heme synthesis, is also important as a proteasome interacting protein.
δ-Aminolevulinate dehydratase activity in type 2 diabetic patients and its association with lipid profile and oxidative stress.
Moretto et al., Santa Maria, Brazil. In Clin Biochem, 2011
association between oxidative stress, abnormalities on lipid profile, distribution of body fat and delta-ALA-D activity inhibition; the enzyme is more oxidized in the DM2 patient
Comprehensive analysis of 5-aminolevulinic acid dehydrogenase (ALAD) variants and renal cell carcinoma risk among individuals exposed to lead.
Moore et al., Bethesda, United States. In Plos One, 2010
A common genetic variation in ALAD may alter the risk of renal cell carcinoma
The relevance of the individual genetic background for the toxicokinetics of two significant neurodevelopmental toxicants: mercury and lead.
Hengstschläger et al., Vienna, Austria. In Mutat Res, 2010
Delta-aminolevulinic acid dehydratase (ALAD), vitamin D receptor (VDR) and hemochromatosis (HFE) gene variants are the only well-established susceptibility markers of lead toxicity in humans.
[Lead exposure markers and related susceptibility genes based on different people].
Qu et al., Shanghai, China. In Wei Sheng Yan Jiu, 2010
Besides ALAD, VDR, HFE genes, the polymorphisms of TF gene and oxidative-stress related genes (Rac2, GPx1, XDH) have been discovered recently to affect lead internal exposure level as well.
[Genetic aspects of hypertensive effect of lead].
Skoczyńska, Wrocław, Poland. In Med Pr, 2007
The interaction between Pb toxicity and ALAD gene polymorphisms on hematopoesis is observed in workers occupationally exposed to lead.
Import of host delta-aminolevulinate dehydratase into the malarial parasite: identification of a new drug target.
Padmanaban et al., India. In Nat Med, 2000
The parasite Plasmodium berghei imports the enzyme delta-aminolevulinate dehydratase (ALAD), and perhaps the subsequent enzymes of the pathway from the host red blood cell to sustain heme synthesis.
Treatment of hereditary tyrosinaemia type I by inhibition of 4-hydroxyphenylpyruvate dioxygenase.
Strandvik et al., Göteborg, Sweden. In Lancet, 1992
The almost complete inhibition of porphobilinogen synthase in erythrocytes was abolished and the excretion of 5-aminolevulinate decreased to within or slightly above the reference range.
Synthesis of the pyrrole porphobilinogen by sepharose-linked -aminolevulinic acid dehydratase.
Shemin et al., In Science, 1973
delta-Aminolevulinic acid dehydratase from Rhodopseudomonas spheroides was covalently linked to Sepharose 4B, which had been activated with cyanogen bromide.
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