The Formation of Pyridoxal and Pyridoxal 5-Phosphate Hydrazones<sup>1</sup>

Wiegand, Ronald G.

doi:10.1021/ja01601a041

Cited by 44 publications

(10 citation statements)

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“…Evidence has been presented to suggest that the inhibition of glutamic acid decarboxylase and GABA-transaminase is the result of interaction be tween formyl group of pyridoxal phosphate and hydrazides (11,12). Actually in vitro studies have demonstrated that isoniazid, one of the hydrazides, easily combines with pyridoxal phosphate to form the corresponding hydrazone (13). Our present experi ments failed to present direct in vivo demonstration of the pyridoxal phosphate com plexes.…”

Section: Discussioncontrasting

confidence: 76%

Correlation Between Convulsive Action and Metabolism of Isoniazid

Saito¹,

Yoshikawa²,

Kinoshita³

et al. 1964

Japanese Journal of Pharmacology

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It is well known that the animal, after a large dose of isoniazid, has a short series of clonic movements followed by a tonic convulsion with a sustained contraction of all muscles.The seizures are characterized by a relatively prolonged interval of time between the administration of the drug and the onset of epileptiform seizures (1, 2).In our preceding paper (3), it has been described that this latent period differs with routes of administration and may be dependent on the isoniazid level in the central nervous system.Assuming that there existed a critical concentration in regard to the brain level of isoniazid, it would reasonably be considered that the convulsion does not appear until the brain level exceeds this critical point, even if an animal received isoniazid sufficient to cause a maximal seizure.Many reports, however, revealed that isoniazid undergoes a considerable metabolic change within a few hours after the administration to man and experimental animals (4, 5). Therefore, it is felt that an investigation of the distribution and metabolic pattern of isoniazid in the animals under the drug-induced seizures may serve to determine if any correlation existed between the convulsive action and the metabolism of this com pound. The present paper describes distribution experiments in cats receiving a convulsive dose of isoniazid and also describes metabolic experiments carried out with mice receiv ing 14C-labelled isoniazid.MATERIALS AND METHODS Examination of brain for isoniazidCats, weighing 2 to 4 kg, were injected intraperitoneally with 150 or 250 mg/kg of isoniazid. In the first group, the animals were sacrificed 20 or 40 minutes after the injection. The central nervous tissues were removed and subjected to chemical analysis. In the second group, the animals were killed when the first seizure appeared. In the third group, the animals received 250 mg/kg. The tissues were removed immediately

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Section: Discussioncontrasting

confidence: 76%

Correlation Between Convulsive Action and Metabolism of Isoniazid

Saito¹,

Yoshikawa²,

Kinoshita³

et al. 1964

Japanese Journal of Pharmacology

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“…The rationale for selecting PLP as a ligand to tether onto side chains of bPEI was primarily based on the following assumptions, (i) being a biocompatible ligand, PLP would serve as a source of aldehyde function, (ii) the coupling of primary amines with aldehyde function of PLP followed by in situ reduction would decrease the density of primary amines in modied polymers, thereby, signicantly improving the cell viability, (iii) introduction of a hydrophobic ligand would facilitate the selfassociation of the polymeric chains (intra-and intermolecularly), which would result in the formation of particles in the nanometer range suitable for efficient entry into the cells, (iv) the presence of sodium phosphate (salt) in the aromatic ring structure would further stabilize the intra-and intermolecular hydrophobic interactions, 34,35 (v) enhanced interactions with the lipidic constituents of the cell membranes would augment the endocytosis and internalization of the DNA complexes, (vi) a decrease in the positive charge density would diminish the non-specic interactions, and (vii) the catalytic effect of the hydroxyl and phosphate groups in PLP would enhance the rate of formation of Schiff base. 36,37 Keeping these points into consideration, we synthesized a small series of phosphopyridoxyl-PEI (PPyP) polymers and studied their cytotoxicity and capability to carry nucleic acids in vitro and in vivo.…”

Section: Resultsmentioning

confidence: 99%

Self-assembled amphiphilic phosphopyridoxyl-polyethylenimine polymers exhibit high cell viability and gene transfection efficiency in vitro and in vivo

et al. 2013

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“…Interactions of INH with endobiotics in the liver provide novel insights into the underlying mechanisms of INH hepatotoxicity (Li et al, 2016). INH directly reacts with various ketones and aldehydes like pyruvic acid (PA) and pyridoxal (PL) to form INH-pyruvic acid (INH-PA) adduct and INH-pyridoxal (INH-PL) adduct, respectively (Zamboni and Defranceschi, 1954;Wiegand, 1956;Li et al, 2011;. INH can also conjugate with fatty acids and lead to accumulation of acylcarnitines in mouse liver (Li et al, 2016).…”

Section: Downloaded Frommentioning

confidence: 99%

Cell Type–Specific Roles of CD38 in the Interactions of Isoniazid with NAD⁺in the Liver

Zhu

Tung

et al. 2020

Drug Metab Dispos

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β-nicotinamide adenine dinucleotide (NAD +) is a critical molecule that is involved in multiple cellular functions. The cluster of differentiation (CD) 38 is a multifunctional enzyme with NAD + nucleosidase activity. Our previous work revealed the CD38-dependent interactions of isoniazid (INH), an anti-tuberculosis drug, with NAD + to form INH-NAD adduct. In the current work, our metabolomic analysis discovered a novel NAD + adduct with acetylisoniazid (AcINH), a primary INH metabolite mediated by N-acetyltransferase (NAT), and we named it AcINH-NAD. Using Nat1/2(-/-) and Cd38(-/-) mice, we determined that AcINH-NAD formation is dependent on both NAT and CD38. Because NAT is expressed in hepatocytes (HP), whereas CD38 is expressed in Kupffer cells (KC) and hepatic stellate cells (HSC), we explored cell type-specific roles of CD38 in the formation of AcINH-NAD as well as INH-NAD. We found that both INH-NAD and AcINH-NAD were produced in the incubation of INH or AcINH with KC and HSC, but not in HP. These data suggest that hepatic non-parenchymal cells, such as KC and HSC, are the major cell types responsible for the CD38-dependent interactions of INH with NAD + in the liver.

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The Formation of Pyridoxal and Pyridoxal 5-Phosphate Hydrazones¹

Cited by 44 publications

References 1 publication

Correlation Between Convulsive Action and Metabolism of Isoniazid

Correlation Between Convulsive Action and Metabolism of Isoniazid

Self-assembled amphiphilic phosphopyridoxyl-polyethylenimine polymers exhibit high cell viability and gene transfection efficiency in vitro and in vivo

Cell Type–Specific Roles of CD38 in the Interactions of Isoniazid with NAD⁺in the Liver

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The Formation of Pyridoxal and Pyridoxal 5-Phosphate Hydrazones1

Cited by 44 publications

References 1 publication

Correlation Between Convulsive Action and Metabolism of Isoniazid

Correlation Between Convulsive Action and Metabolism of Isoniazid

Self-assembled amphiphilic phosphopyridoxyl-polyethylenimine polymers exhibit high cell viability and gene transfection efficiency in vitro and in vivo

Cell Type–Specific Roles of CD38 in the Interactions of Isoniazid with NAD+in the Liver

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The Formation of Pyridoxal and Pyridoxal 5-Phosphate Hydrazones¹

Cell Type–Specific Roles of CD38 in the Interactions of Isoniazid with NAD⁺in the Liver