• The Korean Journal of Zoology
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• v.33 no.4
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• pp.493-498
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• 1990

The effects of an antimetabolite, 6-aminonicotinamide (6-AN) on the levels of enzymes and metabolites in rabbit serum were investigated. The intraperitoneal administration of 6-AN (multiple doses of l5mg/kg body weight) gave tise to a remarkable increase in glucose and cholesterol levels but did not exert any appreciable influence on the concentration of albumin and total protein. Alkaline phosphatase activity was significantly reduced by administration of 6-AN, whereas creatine phophokinase, serum glutamic oxaloacetate transaminase and serum glutamic pyruvate transaminase activities were matkedly enhanced. Nevettheless, the levels of Ca, P, Na, K, Cl and Co were not affeded to any extent by 6-AN.

• Applied Microscopy
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• v.27 no.3
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• pp.281-293
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• 1997

The effects of antimetabolite, 6-aminonicotinamide (6-AN), on ultrastrudural changes in the spinal cord of golden hamster were investigated. Intraperitoneal administration of 6-AN (10 mg/kg body weight) every two days gave rise to a marked reduction of about $30\sim40%$ in body weight after $26\sim28$ days ($13\sim14th$ injection). In the lesions of the spinal cord, neuroglial cells such as astrocytes and oligodendrocytes were severely damaged, but neurons and blood vessels were not affected by 6-AN. The myelin sheath was also affected by 6-AN. Vacuoles observed in the lesions were produced by the swelling and degenerating changes of neuropils and neuroglial cells. Numerous swollen mitochondria and cisterns of rough endoplasmic reticulum were observed in the watery cytoplasm of damaged neuroglial cells, but intermediate filaments were well preserved. Especially in the damaged astrocytes, the outer nuclear membrane were partially swollen and formed a halfmoonlike structure. It is suggested that as well as the multivesicular bodies protruding from the swollen dendrites, the conjugation of adjacent vacuoles also participated in the formation of large vacuoles.

• The Korean Journal of Zoology
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• v.35 no.1
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• pp.23-28
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• 1992

The effects of an antimetabolite, 6-aminonicotinamide (6-AU) on the levels of glucose, glycogen, catechoamines and mucleotides in mice brain were investigated. The level of glucose in the blood starts increasing from 3 h after administration of 6-AU while those in the brain tissue start increasing from 9 h after administration of 6-AN. The concentration of brain glvcogen remained unchanged at all time points except 11h. The level of epinephrine in the brain was found to reach maximum value at initial 3 h following 6-AU administration, after urhich it started dec$\ulcorner$easing si역서cantle. The Brvel of brain norepinephrine remained virtually unchanged before 24 h time point at which it starts decreasing significantly. ATP, CTP, UMP and UTP levels were significantly reduced but AMP and CMP levels urere not affected.

• The Korean Journal of Zoology
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• v.39 no.3
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• pp.299-306
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• 1996

The effects of antimetabolite 6-aminonicotinamide on levels of soluble proteins, free amino acids and protease activity in various tissues of quail have been in vestigated. The levels of soluble proteins m liver, heart and pectoral muscle were markedly lowered and the specific activity of protease in kidney and pectoral muscle was markedly increased. The concentrations of aspartic acid / asparagine, alanine, valine, methionine, isoleucine, leucine and lysine in the liver were markedly increased. En the kidney the concentrations of aspartic acid I asparagine, arginine, threonine, alanine, proline and lysine were markedly increased but those of glutamic acid I glutamine were decreased. The concentrations of glutamic acid / glutamine and serine in the heart were reduced but those in glycine and methionine were increased. In the pectoral muscle the concentration of arginine was decreased but the concentration of alanine and threonine was increased. The overall results suggest that antimetabolite 6-aminonicotinamide may act to enhance concentrations of amino acids related to the generation of energy and to depress the biosynthesis of some specific amino acids.

• Applied Microscopy
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• v.27 no.2
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• pp.177-187
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• 1997

Hydrocephalus is induced experimentally in prenatal and suckling animals following an injection of 6-aminonicotinamide (6-AN). The most remarkable characteristic of these animals is aqueduct stenosis caused by swellings of the ependymal cells and subependymal cells in the periaqueductal gray matter and the central canal of the spinal cord. The present study was undertaken to investigate the morphological changes of the ependymal cells in the central canal of the spinal cord of 3.5 months old hamster after treatment with 6-AN. Intraperitoneal administrations of 6-AN (10 mg/kg body weight) every two days gave rise to partial central canal stenosis of the spinal cord after 27-29 days (13-l4th injection), but cilia and microvilli were located in the strictural area of the con#rat canal. The vacuolations in the ependymal cells were not observed and degenerating changes of intracellular organelles of the ependymal cells did not occur, so that the ependymal cells lining the central canal of the hamster spinal cord were not affected by 6-AN. But the present study demonstrate that 6-AN causes to create numerous vacuoles in the subependymal area of the central canal. Although the vacuoles were well developed in the neuroglial cells and the neuropils of the subependymal area, the neurons were not affected by 6-AN. These results strongly suggests that partial central canal stenosis occurred by 6-AN was due to vacuolations and swellings of the neuroglial cells and nueropils in the subependymal area.

• Biomedical Science Letters
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• v.12 no.3
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• pp.233-240
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• 2006

We investigated enzyme activity and histochemical changes in hind limb of mouse treated with 6-aminonicotinamide (6-AN). The activity of aspartate aminotransferase, alanine aminotransferase and creatine phosphokinase in 6-AN treated group were significantly higher than those of the control and pair-fed groups. Also, the activity of lactic dehydrogenase in 6-AN treated group was the highest among the three groups, whereas that of the pair-fed group were higher than that of the control group. In the 6-AN treated group, oxidative histochemical stains, nicotinamide adenine dinucleotide reductase (NADH), succinyl dehydrogenase (SDH) showed increased scattered fibers in 6-AN treated subsarcolemma. Cytochrome c oxidase (COX) stain showed decreased up to 85% in 6-AN treated fibers. These results demonstrate that 6-AN antagonizes cell metabolism and induces the morphological deformity like the other mitochondrial muscle diseases. Therefore, we suppose that these data would be useful indexes for disclosing the mechanism of mitochondrial muscle disease.

• Applied Microscopy
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• v.38 no.3
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• pp.205-212
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• 2008

In this study morphological changes of the testes of golden hamsters treated with 6-aminonicotinamide (6-AN, 10 mg/kg body weight) in every two days were investigated using light and transmission electron microscopes. After the 7th injection of 6-AN, body weights of hamsters were significantly reduced, and the weight of testes were markedly reduced in the group of hamsters after 5th injections. Degeneration of seminiferous epithelium appeared first in the group receiving 5th injections, which were followed by severe degenerations after the 9th injection. In the degenerated seminiferous epithelium, deep vacuolization, and destruction of spermatogenic cells and Sertoli cells were also oberved. Multinuclear giant cells were also observed in the lumen of destructed seminiferous epithelium. But there were no edematous changes in the interstitial tissue, and the Leydig cells were found to be relatively intact. Therefore, these results show that 6-AN trigger severe morphological alteration of the spermatogenic cells and Sertoli cells, however Leydig cells are unaltered by 6-AN.

• Animal cells and systems
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• v.9 no.4
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• pp.191-198
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• 2005

The effects of 6-aminonicotinamide (6-AN) on viability of IMR32 neuroblastoma cells in the presence of ATP or $NAD^+$ have been investigated. 6-AN caused marked reduction in cell viability and similar observations were also made with cells treated with 6-AN+ATP. However, cells treated with $6-AN+NAD^+$ showed cell viability similar to untreated cells. Morphologically, 6-AN and 6-AN+ATP treated cells showed loss of neurites, polyhedric shapes, shrinkage of cell bodies and formation of lysed cells, while $6-AN+NAD^+$ cells did not show any such changes. The flow cytometry analysis demonstrated that 6-AN increased cell population in $G_0/G_1$ phase and decreased cell population in Sand $G_2/M$ phase following a 72 h exposure. Western blot analysis showed that 6-AN stimulated a substantial increase in the level of the cdk inhibitor $p27^{kip1}$, but lowered the levels of cdk2, cyclin E and p-Rb. However, cdc25A and p53R2 were not significantly affected. Immunofluorscence staining of $p27^{kip1}$, cdk2, cyclin E and p-Rb revealed close correlation between the signal observed in the Western blot analysis. 6AN+ATP treated cells showed similar results obtained with 6-AN treated cells in expression of cdk2, cyclin E, p-Rb proteins and $p27^{kip1}$, $6-AN+NAD^+$ cells showed greater expression of cdk2, cyclin E and p-Rb than those in 6-AN and 6-AN+ATP treated cells. The results suggest that 6-AN induced the $G_0/G_1$ phase arrest in IMR32 neuroblastoma cell lines through the increase of $p27^{kip1}$ and the decrease of cdk2, cyclin E and p-Rb.

• Proceedings of the Zoological Society Korea Conference
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• 2003.08a
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• pp.170.1-170
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• 2003

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 2001.04a
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• pp.30-31
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• 2001

No Abstract, See Full Text