Acetylation

Weber, Wendell W.; Glowinski, Irene B.

doi:10.1016/b978-0-12-380002-2.50015-4

Cited by 10 publications

(4 citation statements)

References 33 publications

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“…On the basis of early work by Price Evans et al (1960) with isoniazid, individuals were classified as either slow or fast acetylators. This polymorphism was found to be controlled by 2 autosomal alleles at a single gene locus, with slow acetylators being autosomal homozygous recessive and fast acetylators heterozygous or homozygous dominant (Weber & Glowinski 1980). In 1970, Perry and co-workers made the interesting observation that their patients with hydralazineinduced DRL were slow acetylators.…”

Section: Acetylationmentioning

confidence: 99%

Drug-Related Lupus

Adams

Hess

1991

Drug Safety

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Adverse side effects to drugs and chemicals in which immune mechanisms may be responsible have been described in drug-related lupus (DRL). The spectrum of drugs that may elicit DRL includes such classes as the hydrazines, arylamines, and chemicals that can be metabolised to amines. The 2 major pathways of metabolism--acetylation and N-hydroxylation--are described in detail. The events leading to autoantibody production are not well understood; however, specific consideration of the genetic makeup of patients who are candidates for treatment with these drugs may help identify those at risk of developing DRL.

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Section: Acetylationmentioning

confidence: 99%

Drug-Related Lupus

Adams

Hess

1991

Drug Safety

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“…The rate of this acetylation is genetically determined and polymorphic in nature-that is, individuals in a population can be distinguished as either 'fast' or 'slow' acetylators on the basis of their ability to convert particular amine and hydrazine drug substrates to their N-acetyl derivatives (Weber & Glowinski, 1980). The genetic basis for the polymorphic acetylation capacity resides with the existence of two major alleles at a single autosomal gene locus governing the production of the hepatic N-acetyltransferase enzyme (EC 2.3.1.5) (Evans et al, 1960;Evans & White, 1964).…”

Section: Introductionmentioning

confidence: 99%

“…The genetic basis for the polymorphic acetylation capacity resides with the existence of two major alleles at a single autosomal gene locus governing the production of the hepatic N-acetyltransferase enzyme (EC 2.3.1.5) (Evans et al, 1960;Evans & White, 1964). Drugs metabolized by this enzyme include isoniazid, procainamide, dapsone, sulphamethazine, phenelzine and hydralazine (Weber & Glowinski, 1980;Lunde et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

A simple test for acetylator phenotype using caffeine.

Grant¹,

Tang²,

Kalow³

1984

Brit J Clinical Pharma

186

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A method is presented for the use of caffeine, in the forms commonly ingested by a large proportion of the world's population, to test for the clinically important acetylation polymorphism. Each of 146 subjects provided a spot sample of urine between 2 and 6 h after coffee, tea or cola soft drink consumption, and the molar ratio of 5‐acetylamino‐6‐ formylamino −3‐methyluracil (AFMU) to 1‐methylxanthine (1X) was determined by a simple h.p.l.c. assay. The ratio afforded segregation of three apparent modes of acetylation capacity in this population, in concordance with a standard sulphamethazine phenotyping procedure and with other methods using controlled caffeine intake and urine collections. The day‐to‐day consistency of the method was established in eight selected subjects.

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“…Some drugs such as sulfamethazine, hydralazine, p-aminosalicylic acid, p-aminobenzoic acid (PABA), isoniazid, phenelzine, procainamide and some toxic agents such as aminofluorene, benzidine agents a-naphthylamine, (3-naphthylamine and methylene bis-2-chloroaniline are conjugated with an acetyl group [Weber, 1973;Glowinski et al, 1978;Weber and Glowinski, 1980]. The usual consequence of ace tylation is a loss of the pharmacological or toxicological activity.…”

Section: Introductionmentioning

confidence: 99%

Acetyltransferase in Humans: Development and Tissue Distribution

Pacifici

Franchi²,

Colizzi³

et al. 1986

Pharmacology

109

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Acetyltransferase with p-aminobenzoic acid (PABA) as substrate was investigated in the cytosolic fraction of the placenta, liver, adrenals, lungs, kidneys, intestine from human fetuses and the liver, lungs, kidneys and intestinal mucosa from adult subjects. All tissue specimens assayed catalyzed the acetylation of PABA at a significant rate. The activity (expressed as nmol of product formed/min/mg protein; mean ± SE) was 1.10 ± 0.59 in the fetal liver, 0.66 ± 0.04 in the placental and 3.87 ± 0.53 in the adult liver cytosol. Among the fetal tissues, the adrenals had the highest (2.36 ± 0.78) and the gut the lowest activity (0.71 ± 0.11). The acetyltransferase activity (mean ± SE) in the lungs, kidneys and intestinal mucosa from adult subjects was 1.19 ± 0.15; 1.34 ± 0.04 and 3.80 ± 0.34, respectively.

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Acetylation

Cited by 10 publications

References 33 publications

Drug-Related Lupus

Drug-Related Lupus

A simple test for acetylator phenotype using caffeine.

Acetyltransferase in Humans: Development and Tissue Distribution

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