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PubMedDate not supplied

Studies on the effect of penicillin, streptomycin and isonicotinic acid hydrazide on small intestinal oligosaccharidase.

Studies have been done on the effect of Penicillin, Streptomycin and Isonicotinic Acid hydrazide on small intestinal oligosaccharidase and it was observed that the drug penicillin inhibited the enzyme lactase and sucrase by 62.7% and 34.7% respectively, whereas I.N.H. inhibited the enzyme sucrase and maltase by 57.1% and 56.14% respectively. Streptomycin did not show any inhibitory effect on those enzymes. Lactose tolerance test showed impairment of lactose absorption in case of penicillin. Fasting serum sugar level was diminished both in penicillin and streptomycin and the absorption capacity was increased after oral administration of streptomycin.

Animals↗
PubMed1984

Isonicotinic acid hydrazide: early effects on peripheral nerve conduction velocity.

This report describes the effects of short treatments with isonicotinic acid hydrazide (isoniazid), 300 mg/kg/day, on conduction velocity in the rat tail dorsal nerve trunk. After 6 days of continuous treatment, conduction velocity falls significantly for measurements made at 35 degrees C. After 10 days it falls significantly at both 25 degrees C and 35 degrees C. This appears to be the first electrophysiological corroboration of the early neuropathological changes recently observed in isoniazid treated rats and seems to provide evidence that the temperature at which the experiments are made is important in determining conduction velocity changes.

Animals↗
PubMed2003

Usefulness of graphical invariants in quantitative structure-activity correlations of tuberculostatic drugs of the isonicotinic acid hydrazide type.

Quantitative structure-activity relationship (QSAR) studies have been performed for a series of 2-substituted isonicotinic acid hydrazides utilizing theoretical molecular descriptors. 223 topological (topostructural and topochemical) indices along with seven geometrical descriptors were computed for the prediction of antibacterial activity against Mycobacterium tuberculosis. Ridge-regression models assessed by cross-validated R2 have been formulated, and a comparative study on the relative effectiveness of physicochemical vis-à-vis theoretical molecular descriptors performed. The models developed clearly indicate the supremacy of structure-activity over property-activity relationships in the current study and can be used to evaluate the potential tuberculostatic activity of other INH derivatives, real or hypothetical.

Antitubercular Agents↗
PubMed1989

Synthesis and characterization of new chromium(III), vanadium(IV), and titanium(III) complexes with biologically active isonicotinic acid hydrazide.

New complexes of the type [Cr(INH)2Cl2]Cl.2H2O, VO(INH)2Cl2 and TiO(INH)2Cl, where INH = isonicotinic acid hydrazide, have been prepared. The complexes were characterized by infrared and UV-vis spectroscopy, proton nuclear magnetic resonance (NMR) and elemental analyses, molar conductivity and x-ray powder diffraction measurements. For the Cr(III)-complex, the ligand was coordinated through its carbonyl group and amino nitrogen atom; for V(IV)-complex and Ti(III)-complex, the ligand was coordinated through its carbonyl oxygen and heterocyclic nitrogen, respectively. Octahedral geometry has been proposed for all the complexes. The complexes of Cr(III) and Ti(III) showed significant tuberculostatic activity.

Antitubercular Agents↗
PubMed1994

Effect of isonicotinic acid hydrazide on extracellular amino acids and convulsions in the rat: reversal of neurochemical and behavioural deficits by sodium valproate.

We have studied the effect of isonicotinic acid hydrazide (INH), a convulsant agent, on the extracellular levels of amino acids in the hippocampus, and the effect of sodium valproate (VPA) administration in INH-treated rats. INH (250 mg/kg) caused a rapid and sustained decrease in basal levels of GABA, and during this period convulsions of increasing severity were observed. Basal levels of glutamine, taurine, aspartate, and glutamate were unchanged by INH. When VPA was coadministered with INH, basal GABA levels were increased and no convulsions were observed. When transmitter release was evoked using 100 mM K+, the increase in dialysate GABA observed in INH-treated animals was less than that seen in controls and convulsions increased in frequency. K(+)-evoked release of glutamate and aspartate tended to be higher following INH treatment, and in the case of aspartate, this increase was significant. VPA reversed the changes in evoked release of glutamate and aspartate, and release of GABA was considerably greater than that seen in control or INH-treated rats. No drug effect on evoked changes in taurine or glutamine level was seen. These are the first data to show decreased extracellular GABA in conjunction with convulsions in freely moving animals in vivo.

Amino Acids↗
PubMedDate not supplied

Isonicotinic acid hydrazide: an anti-tuberculosis drug inhibits malarial transmission in the mosquito gut.

We studied the transmission-blocking effect of isonicotinic acid hydrazide (INH), a widely used anti-tuberculosis drug, against Plasmodium gallinaceum and Plasmodium berghei. INH-treatment of infected animals did not inhibit parasite development in the blood of the vertebrate host, but did inhibit exflagellation, ookinete formation, and oocyst development in the mosquito. Oocyst development was inhibited in a dose-dependent manner. The ED(50) in the P. gallinaceum/chicken/Aedes aegypti model and P. berghei/mouse/Anopheles stephensi model was 72 and 109 mg/kg, respectively. In marked contrast, in vitro exflagellation and ookinete development were not directly affected by physiological concentrations of INH. We suggest that INH exerts its inhibitory effects on the mosquito stages of the malaria parasite by an indirect, and at present undefined mechanism. Further elucidation of the mechanism how INH inhibits parasite development specifically on mosquito stages may allow us to identify new targets for malaria control strategy.

Aedes↗
PubMed1984

Isonicotinic acid hydrazide induced changes and inhibition in mycolic acid synthesis in Nocardia and related taxa.

The mycolic acid compositions of Nocardia rubra and related bacteria grown in media containing different concentrations of antituberculous isonicotinic acid hydrazide (INH) were determined in detail by gas chromatography-mass spectrometry. On the basis of molecular species composition, average carbon numbers of mycolic acids were calculated. In Nocardia rubra, N. lutea and Rhodococcus rhodochrous IFO-13161, the ratio of mycolic to non-mycolic fatty acids and the average carbon numbers of mycolic acids were decreased at the INH concentrations of higher than 1 microgram/ml, paralleling with the significant inhibition of growth. In above three species the synthesis of longer chain mycolic acids (longer than C44 or C46 ) was inhibited more significantly than shorter homologues such as C38 or C40 . In contrast, neither growth inhibition nor change in corynomycolic acid composition was observed in Corynebacteria xerosis and Rhodococcus rhodochrous IFO-13165 at the concentration region of INH up to 100 micrograms/ml. The direct mass fragmentographic analysis of the trimethylsilylated (TMS) derivatives of mycolic acid methyl esters, monitoring [M-15] ions of individual molecular species, revealed that the chain shortening of total mycolic acid molecule by INH occurred more greatly in more highly unsaturated subclasses than in less unsaturated subclasses. Furthermore, mass fragmentographic analysis, monitoring fragment ions (A) and (B), due to straight chain and branched chain alkyl units, respectively, demonstrated the inhibition of mycolic acids was not attributed to the shortening of alpha-alkyl chain, but to the inhibition of chain elongation of C28 to C32 straight chain meromycolic acids. It was also indicated the amounts of trehalose mono- and di- mycolate (cord factor) decreased significantly with the addition of INH (1 to 20 micrograms/ml) in the above strains. From the results obtained above, INH appeared to inhibit the synthesis of mycolic acids longer than C44 or C46 specifically by inhibiting chain elongation or desaturation of precursor long chain fatty acids longer than C28 or C30.

Actinomycetales↗
PubMed1975

Acetylation of procainamide in man and its relationship to isonicotinic acid hydrazide acetylation phenotype.

To assess the extent of the acetylation of procainamide (PA) to N-acetylprocainamide (NAPA) in man, and its relation to isonicotinic acid hydrazide (INH) acetylation phenotype, the following study was done. Fourteen subjects received 500 mg of PA - HCL orally. INH acetylation phenotype was determined by the serum half-life of INH after 4 mg/kg of INH orally. Each urine voided for 96 hr after procainamide was saved and levels of procainamide and NAPA measured by gas-liquid chromatography. The 14 subjects eliminated 52 plus or minus 4 percent of the dose as procainamide and 16 plus or minus 2 percent of the dose as NAPA. Four fast INH acetylators eliminated 23 plus or minus 3 percent of the dose as NAPA compared to 12 plus or minus 1 percent by the slow acetylators (p smaller than 0.05). The amount of unaltered procainamide excreted by the fast and slow INH acetylators was not significantly different, 50 plus or minus 4 percent and 53 plus or minus 4 percent, respectively. Of the total amount of drug recovered in the urine of the fast and slow INH acetylators, NAPA accounted for 32 percent and 19 percent, respectively (p smaller than 0.01). There appears to be a positive correlation between the ability to acetylate INH and the ability to acetylate procainamide.

Acetylation↗
PubMed1977

Effect of isonicotinic acid hydrazide on the intratumor injection of BCG.

Rats with established subcutaneous tumors were treated by repeated intratumor injections of BCG over a 5-week period. Isonicotinic acid hydrazide (INH) was given to some rats to determine if this drug decreased the effect of BCG on local tumor growth. INH alone had no effect on either survival or tumor volume. Rats treated with either BCG or BCG and INH had prolonged survivals and smaller tumor volumes than did controls rats. In these experiments, INH did not decrease the effect of BCG on local tumor growth. However, the intratumor injection of BCG in rats receiving INH systematically was associated with better survival and smaller tumor volumes compared to the intratumor injection of BCG alone.

Adenocarcinoma↗
PubMed1991

The synergistic effect of isonicotinic acid hydrazide (INH) and griseofulvin (GF) on porphyrin metabolism.

Abnormal porphyrin metabolism can be induced by several chemicals. To investigate the synergistic effect on porphyrinopathy of isonicotinic acid hydrazide (INH) with a low concentration of griseofulvin (GF), the two chemicals were given to mice simultaneously. INH was added to drinking water at a concentration of 0.05%. GF was mixed with feed at a concentration of 0.1%. The mice (dd-y strain) were divided into four groups. Those in group A were fed normally. Group B received only 0.1% GF, group C received only 0.05% INH, and group D received both 0.1% GF and 0.05% INH. The treatment was continued for 13 to 30 weeks. After treatment, the mice were anesthetized and sacrificed. The liver and whole blood were taken for analysis of porphyrins. The results revealed a slight elevation of erythrocytic porphyrins in the groups treated with 0.1% GF or 0.05% INH alone and remarkable abnormalities in the hepatic and erythrocytic porphyrin levels of the group simultaneously treated with both chemicals. These results show that INH itself may have a small potential for the induction of porphyric abnormalities, and that the administration of INH with a low concentration of GF induces marked porphyrinopathy in dd-y strain mice.

Animals↗
PubMed1991

Isonicotinic acid hydrazide inhibits cell population growth during teratogenesis of chick embryo.

In chick embryos treated with a 4 hr pulse of 7.2 X 10(-5) M isonicotinic acid hydrazide (INH) the cell population growth is inhibited with an increased population doubling time. Teratogenised blastoderm cells complete their ongoing cell cycle and arrest in G1 phase. A chase with an equimolar concentration of pyridoxal-5-phosphate restores the growth rate after a lag of 4 hr equivalent to the duration of treatment with INH. Presumptive mesoblast cells invaginated through the primitive streak and neuroectoblast cells induced prior to the application of INH differentiate, while the teratogen inhibits morphogenesis and organization of organ primordia.

Animals↗
PubMed2004

Crystalline inclusion compounds constructed through self-assembly of isonicotinic acid and thiocyanato coordination bridges.

The synthesis, crystal structures, inclusion ability, and structural robustness of novel crystalline inclusion compounds of [Ni(SCN)2(isoH)2].xG (isoH = isonicotinic acid; G = aromatic guest) are described. The inclusion compounds are constructed by stacking identical 2D host layers that consist of SCN-, isoH, and Ni2+ with van der Waals contact separation. In the layer, two types of rectangular cavities (A-type and B-type) are formed, and the guests are included in the former cavity. The inclusion compounds were categorized into four stacking modes according to the difference in the stacking mode of the layers. A systematic investigation of the crystal structures of the 21 inclusion compounds clarified the close relationship between the molecular structure of the guest and the resultant stacking mode of the layers.

Journal Article↗