Disease relevance of C07585

• The influence of NAT2 genotypes on the plasma concentration of isoniazid and acetylisoniazid in Chinese pulmonary tuberculosis patients [1].
• Isoniazid and its metabolites including acetylisoniazid, acetylhydrazine, diacetylhydrazine, isonicotinic acid and hydrazine were examined for their potential neurotoxic effects in cultured mouse dorsal root ganglion (DRG) neurons and mouse neuroblastoma x DRG neuron hybrid cell line N18D3 [2].

High impact information on C07585

• Genetically determined enzyme activity was assessed indirectly by calculating the metabolic ratio (parent drug/metabolite in 8-hour urine for CYP2D6 and P450MEPH and N-acetylisoniazid/isoniazid in plasma for N-acetyltransferase) after oral administration of the parent compounds [3].
• The plasma concentrations of isoniazid and its hydrazino metabolites, acetylisoniazid, acetylhydrazine and diacetylhydrazine, were measured by gas chromatography-mass spectrometry in 12 healthy subjects after the ingestion of 300 mg of isoniazid [4].
• The slow phenotype, defined as an acetylation ratio (acetylisoniazid/isoniazid) of less than 2.0, was observed in 13 (14.3%) of the 91 healthy subjects, and in 20 (28.2%) of the 71 bladder cancer patients; the difference between the two groups is significant (p < 0.05) [5].
• The temporal variation in the pharmacokinetics of a single dose administration of isoniazid (INH) and its major metabolite, N-acetylisoniazid (AINH), was investigated at 0900 and 2100 in rats synchronized to a 12-hr light-dark cycle [6].
• A method for the determination of rifampicin, desacetylrifampicin, isoniazid, and acetylisoniazid by high-performance liquid chromatography and using the same extract of the same sample is reported [7].

Biological context of C07585

• Coadministered acetylisoniazid had no effect on acetylation [8].
• 1. The pharmacokinetics of isoniazid and acetylisoniazid in plasma and saliva were compared following administration of oral and intravenous doses (200 mg) to healthy volunteers and patients [9].
• We studied the relationship between NAT2 genotype and INH and its metabolite acetylisoniazid (AcINH) concentration in Chinese people [1].
• To investigate this postulated mechanism we studied the kinetics of the metabolism of acetylisoniazid in a slow and a rapid acetylator prior to and after rifampicin administration [10].

Anatomical context of C07585

• Determination of rifampicin, desacetylrifampicin, isoniazid and acetylisoniazid by high-performance liquid chromatography: application to human serum extracts, polymorphonucleocytes and alveolar macrophages [7].
• In order to explore the exact mechanism of INA formation in the hepatocytes, an HPLC assay for INA in the presence of INH and acetylisoniazid was developed [11].

Associations of C07585 with other chemical compounds

• The ethanol dosage regimen used resulted in peak blood ethanol concentrations between 78 mg/l and 103 mg/l. There was no significant difference in area under the curve, half-life of elimination or the ratio of acetylisoniazid to isoniazid (AcINH/INH) in the sample withdrawn 3 h after isoniazid dose [12].
• The tissue levels of isoniazid, acetylisoniazid, acetylhydrazine, 1,2-diacetylhydrazine and hydrazine were determined by mass fragmentography using a gas chromatograph-mass spectrometer equipped with a multiple ion detector-peak matcher [13].

Analytical, diagnostic and therapeutic context of C07585

• Plasma concentrations of isoniazid and its metabolite, acetyl-isoniazid, were determined by HPLC analyses at various post-dose times [14].

References