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PubMed1976

Comparative studies on the influence of dimethylsulfoxide (DMSO) on reversion to sensitivity to isonicotinic acid hydrazide (INH) and rifampicin (RMP) in resistant strains of tubercle bacilli.

Results of continuing studies on the influence of dimethylsulfoxide (DMSO) on reversion of sensitivity to rifampicin (RMP) and isonicotinic acid hydrazide (INH) in tubercle bacilli are reported. Nineteen strains of RMP-resistant bacilli, and 61 strains of IHN-resistant bacilli were studied. Reversion to INH sensitivity was obtained in 19 of the 61 resistant strains examined. Ten strains reverted completely, and 9 partly. All 19 RMP-resistant strains reverted to complete sensitivity.

Dimethyl Sulfoxide↗
PubMed1989

[Inhibition of porphyrin synthesis by isonicotinic acid hydrazide in models simulating porphyria].

Increased activity of haem synthesis key enzyme is a common phenomenon in hepatic porphyrias. Synthase activity of delta-aminolevulinic acid is extensively increased in acute hepatic porphyrias or it can be by means of feedback moderately secondarily increased in their chronic forms. Isonicotinic acid hydrazide (INH) is a competitive inhibitor of delta-aminolevulinic acid synthase as it combines with enzyme co-factor, pyridoxalphosphate (PDX) to form hydrazone. The INH porphyrinstatic effects were verified by testing two experimental models. The yeast model exhibited 5-fold inhibition at 10 mM INH concentration in medium. The chicken germ model after a 10 microM INH dose exhibited 82% inhibition. This inhibition can be eliminated by PDX administration to reach the original porphyrin synthesis at equimolar INH and PDX concentrations. Histological study of transversal chicken liver sections proved that 1 microM INH administration does not result in disturbance of chicken hepatocyte integration. The suggested preparation has the advantage of being commonly manufactured and approved to be used in human medicine.

Animals↗
PubMed1988

Porphyrinostatic effect of isonicotinic acid hydrazide on porphyric chick embryo and yeast.

1. The common feature of "inducible" forms of hepatic porphyria is an increased activity of delta-amino-levulinate/ALA/synthase. 2. As a potential therapeutic procedure, isonicotinic acid hydrazide/INH/as inhibitor of this enzyme, was applied and found to show a porphyrinostatic effect, depending on its concentration, both in yeast and porphyric chick embryo models. 3. Moreover, pyridoxalphosphate/PDX/eliminated the porphyrinostatic effect of INH, depending again on its concentration. 4. Histochemical tests did not demonstrate any significant functional or morphological changes in the chick embryo hepatocytes following INH administration.

5-Aminolevulinate Synthetase↗
PubMed1978

Effect of isonicotinic acid hydrazide-copper complex on Rous sarcoma virus and its genome RNA.

The copper complex of the antituberculous drug, insonicotinic acid hydrazide (INH), inhibits the RNA-dependent DNA polymerase of Rous sarcoma virus and inactivates its ability to malignantly transform chick embryo cells. The INH-copper complex binds to the 70S genome RNA of Rous sarcoma virus (RSV), which may account for its ability to inhibit the RNA-dependent DNA polymerase. The complex binds RNA more effectively than DNA in contrast to M-IBT-copper complexes, which bind both types of nucleic acids equally. The homopolymers, poly rA and poly rU, are bound by the INH-copper complex to a greater extent than poly rC. Isonicotinic acid hydrazide alone and CuSO4 alone bind neither DNA, RNA, poly (rA), poly (rU), nor poly (rC). However, CuSO4 alone binds poly (rI); INH alone does not. In addition to viral DNA synthesis, chick-embryo cell DNA synthesis is inhibited by the INH-copper complex. The extent of inhibition of cellular DNA synthesis is greater than that of cellular RNA and protein synthesis. No selective inhibition of transformation in cells previously infected with Rous sarcoma virus is observed.

Avian Sarcoma Viruses↗
PubMed2003

Reactivity of tracheal smooth muscles in albino rats with experimental diabetes mellitus treated with a new complex compound of oxovanadium (IV) and isonicotinic acid hydrazide.

We studied functional properties of tracheal smooth muscle cells in rats with diabetes mellitus. Reactivity of tracheal smooth muscles increased in rats with experimental alloxan-induced diabetes mellitus. A new complex compound of oxovanadium (IV) and isonicotinic acid hydrazide affected reactivity of tracheal smooth muscles in albino rats with experimental type I diabetes mellitus. This new organic vanadium-containing compound reduced contractility of tracheal smooth muscles in rats and potentiated relaxation of smooth muscle cells in the trachea in response to exogenous nitric oxide.

Alloxan↗
PubMed1988

Comparison between serum isonicotinic acid hydrazide (INH) levels and urinary sulfadimidine (sulfamethazine) acetylation as predictors of INH acetylator status.

The acetylator status of 40 children with pulmonary tuberculosis was investigated by (1) sulfadimidine (SDM; sulfamethazine) acetylation test in urine and (2) estimation of isonicotinic acid hydrazide (INH) levels. The antimode was at 70% based on the frequency distribution of SDM acetylation. Children acetylating less than 70% of administered SDM were taken as slow acetylators while those with more than 70% as rapid acetylators. The serum INH antimode was at 0.85 micrograms/ml. Thus serum values less than 0.85 micrograms/ml categorised a child as rapid and those with more than 0.85 micrograms/ml as slow acetylators. The sensitivity of these two methods was similar with a correlation coefficient r = 0.64. Thus the determination of the type of acetylator by SDM acetylation test is equally reliable and technically simpler and is recommended instead of INH serum concentration.

Acetylation↗
PubMed2001

Isonicotinic acid hydrazide induced anagen effluvium and associated lichenoid eruption.

A 32 year-old woman developed generalised lichenoid eruptions on her body followed by diffuse loss of scalp hair of the anagen effluvium type. She was receiving several anti-tubercular drugs, including rifampicin, isonicotinic acid hydrazide (INH), pyrazinamide, and ethambutol, for abdominal tuberculosis. INH, which is a leading cause of drug eruptions in the above group of drugs was withdrawn. However, the other antitubercular drugs were continued along with 40 mg of prednisolone in a single daily morning dose. The latter was discontinued slowly over a period of 10 weeks. There was complete recovery of hair loss and the regrowth started after 12 weeks of alopecia. Such anagen effluvium with lichenoid eruption following INH therapy has not been observed previously. The complete recovery from anagen effluvium is difficult to explain, but it could have been because of the early initiation of corticosteroid.

Adult↗