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PubMed1990

Detection of IgE antibodies specific to isonicotinic acid hydrazide and its metabolite by enzyme-linked immunosorbent assay and the mechanism of sensitization by inhalation or ingestion of this compound.

A female hospital pharmacist and a nurse developed occupational asthma due to the inhalation of isonicotinic acid hydrazide (INH) powder. The mechanism of sensitization was examined in this study. Furthermore, IgE antibodies specific to INH and isonicotinic acid (INA), the major metabolite of INH, were examined by means of enzyme-linked immunosorbent assay (ELISA). IgE anti-INH antibody activity was detected by ELISA in sera from 5 out of 8 hospital workers who inhaled INH powder during the handling of INH, and in sera from 10 out of 142 tuberculosis patients receiving oral INH. IgE anti-INA antibody activity was detected in sera from 3 of the 8 hospital workers, and from 7 of the 142 tuberculosis patients. Neither IgE anti-INH nor anti-INA antibody activity was detected in sera from 45 patients with asthma or from 42 healthy volunteers. The specificity of the IgE antibodies and the cross-antigenicity between INH and INA were confirmed by ELISA inhibition studies. Our results indicate that sensitization to INH can occur not only by inhalation but also by oral administration, and that the asthmatic symptoms of the patients were caused by an IgE antibody specific to INH as a hapten.

Administration, Inhalation↗
PubMed1994

High-performance liquid chromatography with UV detection and diode-array UV confirmation of isonicotinic acid hydrazide in cattle milk.

A method for the determination of isonicotinic acid hydrazide (isoniazid) in milk was developed. Milk was deproteinized with trichloroacetic acid. Isoniazid was condensed with cinnamaldehyde and assayed on a reversed-phase HPLC system, with good sensitivity and accuracy (10 micrograms/l) with UV detection at 330 nm. Use of solid-phase extraction with a C18 cartridge allows the detection limit to be lowered to 0.1 microgram/l with UV detection and confirmation of isoniazid hydrazone from the diode-array UV spectrum.

Animals↗
PubMed1994

Apparent hydroxyl radical generation without transition metal catalysis and tyrosine nitration during oxidation of the anti-tubercular drug, isonicotinic acid hydrazide.

Aromatic hydroxylation and formation of thiobarbituric acid-reactive substances occurred in a mixture of isonicotinic acid hydrazide (isoniazid) and catalase. Since these reactions were stimulated by phytic acid (a potent metal chelator), rather than inhibited, transition metal-catalysed hydroxyl radical generation was not implicated. Hydroxylation also occurred with isoniazid and phytic acid in the absence of catalase, albeit to a lesser extent. The independent effects of catalase and phytic acid are related to their abilities to catalyse isoniazid oxidation. In the presence of tyrosine, both the isoniazid/phytic acid system and authentic peroxynitrite generated dityrosine. Authentic peroxynitrite, as well as a phytic acid-mediated isoniazid oxidation product, have absorbance maxima at 302 nm. The yield of this isoniazid-derived product increased with pH and in the presence of a superoxide-generating system. A good correlation existed between absorbance at 302 nm and aromatic hydroxylation. Acid-induced decomposition of the 302 nm absorbance in the presence of superoxide dismutase led to the formation of a product absorbing in the same region as peroxynitrite-modified superoxide dismutase (350 nm at acid pH). Catalase catalysed peroxynitrite-mediated, as well as isoniazid/phytic acid-mediated tyrosine nitration, which was accompanied by Compound II formation (ferryl-catalase) in both cases. We postulate that peroxynitrite or a similar species is formed during isoniazid oxidation.

Catalase↗
PubMed1977

[Toxicology of a polymerized modification of isonicotinic acid hydrazide].

The biologic side effects were studied of a polymer of isonicotinic acid hydrazide (PINH) synthesized on the basis of the copolymer vinylpyrrolidone and crotonaldehyde. The influence of dosage and conditions of administration as a functional and morphologic indicator in animals were also investigated. Threshold dosage and optimal conditions of administration in clinical practice are recommended.

Animals↗
PubMed1996

In vivo inhibition of kynurenine aminotransferase activity by isonicotinic acid hydrazide in rats.

It is known that the anti-tuberculosis drug, isonicotinic acid hydrazide (INH), causes pellagra, a niacin deficiency syndrome, and peripheral neuritis in humans. We investigated the effects of INH on the metabolism of tryptophan to niacin in rats fed on a niacin-free diet. The activity of kynurenine aminotransferase was significantly inhibited by feeding a diet containing INH and by an injection of INH, and the urinary excretion of xanthurenic acid, the side-reaction product of the conversion pathway of tryptophan to niacin, was below the limit of detection. The inhibition of kynurenine aminotransferase and the resulting decreased formation of xanthurenic acid generally mean a higher conversion ratio of tryptophan to niacin. However, the conversion ratio was no different between the control and INH groups.

Animals↗
PubMed1980

An evaluation of the potential use of isoniazid, acetylisoniazid and isonicotinic acid for monitoring the self-administration of drugs.

1. The possibility of using minute doses of the antituberculosis drug isoniazid (INH) or of its metabolites acetylisoniazid (AcINH) or isonicotinic acid (INA) as innocuous markers for monitoring patient compliance has been investigated. 2. The ingestion of these colourless and tasteless compounds can readily be demonstrated using a sensitive and specific colorimetric method for detecting INA and its metabolite isonicotinylglycine (INAG) in the urine that is rapid and simple to perform. 3. Studies on the kinetics of the urinary elimination of INA and INAG after the ingestion of 6 mg doses of either INH, AcINH or INA by small groups of volunteers indicated the potential suitability of INH or AcINH for monitoring daily or twice-daily self-medication and the appropriateness of INA as a marker for investigating the compliance of drugs prescribed for thrice-daily ingestion. 4. More extensive studies showed that over 99% of the urine samples collected within 18h of dosage with 6 mg INH would give positive results when tested for the presence of INA and INAG, and that doses of 2-6 mg INH could readily by incorporated into capsules or tablets and used as markers for monitoring the ingestion of the antituberculosis or antileprosy drugs dapsone, thiacetazone, ethionamide or prothionamide, or the antihypertensive oxprenolol. Such doses are less than a fiftieth of the normal therapeutic INH dose used in the treatment of tuberculosis. 5. Evidence is presented that INH, AcINH and INA possess most of the characteristics that one would hope to find in a marker for monitoring compliance including very limited inter-individual variability in the rates at which they are converted to the compounds being detected in the urine.

Glycine↗
PubMed1994

Different oxidative pathways of isonicotinic acid hydrazide and its meta-isomer, nicotinic acid hydrazide.

1. Superoxide was generated during the auto-oxidation of the antituberculous drug, isonicotinic acid hydrazide (INH), but not with its meta-isomer, nicotinic acid hydrazide (NH). During Fe(3+)-stimulated oxidation of INH and NH, aromatic hydroxylation occurred which was inhibited by the chelating agent, phytic acid. 2. A mixture of myeloperoxidase (MPO) and a hydrazide induced formation of compound III (oxyperoxidase) and aromatic hydroxylation which was stimulated by phytic acid. INH was considerably more potent than NH. 3. Co-oxidation of a hydrazide and thyroxine (T4) in the MPO system resulted in the formation of a pink-coloured product (maximum absorbance at 504 nm) which was more stable with NH than with INH. 4. The hydrazides and Cl- acted synergistically on MPO haem modification when co-oxidised in the MPO-H2O2 system. INH was more destructive than NH. 5. The different oxidative pathways of the hydrazides are consistent with the fact that an acyl intermediate of INH, unlike that of NH, is resonance stabilized.

Carcinogens↗
PubMed1956

Coccidioidomycosis; treatment with isonicotinic acid hydrazide.

Since coccidioidal granulomas are histologically indistinguishable from tuberculous granulomas, a long course of isonicotinic acid hydrazide therapy was tried experimentally in three cases of coccidioidomycosis, with good results. In two cases the disease was far advanced and prognosis poor before INH therapy was begun. In one case the disease was mild and symptoms abated after a short course of small doses of INH. It recurred when INH therapy was discontinued, and again resolved when larger doses of INH were given over a longer period.INH seemed to have an effect on appetite also, although the patients were taking B-complex vitamins both before and during INH treatment. The three patients ill with coccidioidomycosis averaged a weight gain of four and a half pounds a month during the period of INH therapy. Six well persons who were underweight and lacked appetite were given INH without other drugs, and they then had an increase in appetite and in weight.

Coccidioidomycosis↗
PubMed2004

Antimycobacterial constituents from Juniperus procera, Ferula communis and Plumbago zeylanica and their in vitro synergistic activity with isonicotinic acid hydrazide.

The synergistic activity of antimycobacterial constituents from Saudi plants was evaluated in combination with isonicotinic acid hydrazide (INH) against four atypical organisms, namely, Mycobacterium intracellulare, M. smegmatis, M. xenopei and M. chelonei. The potency of INH was increased four-fold, using an in vitro checkerboard method, against each mycobacteria when tested with a subtoxic concentration of the totarol, isolated from J. procera. The MIC values of totarol, ferulenol (from Ferula communis) and plumbagin (from Plumbago zeylanica) were thus lowered from 1.25-2.5 to 0.15-0.3 microg/mL due to synergism with INH. When tested against the resistant strain of M. tuberculosis H37Rv, plumbagin and 7beta-hydroxyabieta-8,13-dien-11,12-dione exhibited inhibitory activity at <12.5 microg/mL, while others were inactive at this concentration.

Antitubercular Agents↗
PubMed1987

Isonicotinic acid hydrazide as an antigen.

Detection by in vitro serologic techniques of circulating antibody directed against isonicotinic acid hydrazide (INH, known as isoniazid) in humans has not been reported. In the past few months, however, sera from a patient with a recent history of isoniazid hypersensitivity of the immediate type have been studied, and reaginic antibodies (IgE) specific to INH were detected by means of an enzyme-linked allergosorbent test. Preliminary enzyme-linked allergosorbent tests also demonstrated that INH-specific IgE occurred in the serum of two of 150 patients with tuberculosis who had been treated with INH.

Adult↗
PubMed1977

Inactivation and inhibition of Rous sarcoma virus by copper-binding ligands: thiosemicarbazones, 8-hydroxyquinolines, and isonicotinic acid hydrazide.

We have shown that three types of copper-binding ligands, thiosemicarbazones, 8-hydroxyquinolines, and isonicotinic acid hydrazide and their copper complexes, inactivate the transforming ability of RSV and inhibit its RNA-dependent DNA polymerases. Three other compounds, 2-pyridine thiosemicarbazone, 1-formyl isoquinoline thiosemicarbazone, and diphenyl thiocarbazone inhibit transformation by RSV intracellularly. Most but not all of these compounds bind to nucleic acids in the presence of copper, which may be important in their mode of action.

Avian Sarcoma Viruses↗