• 한국동물학회지
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• 제33권4호
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• pp.493-498
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• 1990

Antimetabolited인 6-aminonicotinamide(6-AN)가 토끼의 혈청내 효소 및 대사 물질에 미치는 영향에 관하여 연구하였다. 복강투여시 (l5mg/kg의 체중) 포도당과 콜레스테놀농도는 현저이 증가하였으나 알부민고 총단백질량은 크게 변하지 않았다. Creatine phophokinase,glutamic oxaloacetate transaminase,glutamic pyruvate transaminase 및 alctate dehydrogensenase활성은 매우 증가하였으며 alkaline phosphatase와 Ca, P, Na, K, Cl 및 Co등의 수준은 영향을 받지 않았다.

• Applied Microscopy
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• 제27권3호
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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.

• 한국동물학회지
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• 제35권1호
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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.

• 한국동물학회지
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• 제39권3호
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• pp.299-306
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• 1996

항 대사물질 6-aminonicotinamide가 메추리 조직의 수용성 단백질, 유리 아미노산 및 단백질 가수분해효소에 미치는 영향을 조사하였다. 간(P<0.05), 심장(P<0.01), 흉부근육 조직(P<0.05)의 수용성 단백질의 함량은 대조군에 비해 현저히 감소하였다. 신장과 흉부근육 조직의 단백질 가수분해효소의 비활성도는 대조군에 비하여 현저히 감소하였다. 신장과 흉부근육 조직의 단백질 가수분해효소의 비활성도는 대조군에 비해 현저히 증가하였다. (P<0.05). 간(P<0.05)의 aspartic acid / asparagine, alanine, valine, methionine, isoleucine, leucine, lysine의 농도는 대조군에 비해 증가하였다. 신장(P<0.05)의 acid / asparagine, alanine, threonine, alanine, proline과 lysine은 증가하였으나 glutamic acid / glutamine의 농도는 감소하였다. 심장에서는 glycine과 methionine 농도는 증가하였으나 glutamic acid / glutamine의 농도는 감소하였다. 흉부근육 조직에서는 arginine의 농도는 감소하였으나 (P<0.05) alanine과 threonine의 농도는 증가하였다 (P<0.05). 본 연구 결과는 항 대사물질인6-aminonicotinamide가 유리 아미노산의 농도를 증가시키므로써 기포 물질 대사에 필요한 에너지를 유지하는 것으로 사료된다.

• Applied Microscopy
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• 제27권2호
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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.

• 대한의생명과학회지
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• 제12권3호
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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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• 제38권3호
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• pp.205-212
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• 2008

6-aminonicotinamide (6-AN)의 햄스터 정소에 미치는 영향을 확인하기 위해 실험군에는 체중 kg 당 10 mg의 6-AN을, 대조군에는 동량의 생리식염수를 격일로 복강 투여한 후 정소의 변화를 광학 및 투과전자현미경을 이용하여 관찰하였다. 최초 6-AN 투여 당시의 체중에 비해 7회 투여군부터 유의하게 체중이 감소하였으며, 정소 중량의 감소는 5회 투여시 크게 감소하여 이후 비슷한 양상을 보였다. 정세관상피의 퇴행변화는 5회 투여군부터 나타나기 시작하여 9회 투여군부터는 대부분의 정세관이 심하게 손상을 받은 것으로 나타났다. 손상을 받은 정세관에서 정세관상피를 이루는 정자발생세포 및 지지세포 모두 심한 공포화에 따른 세포의 파괴를 뚜렷하게 관찰할 수 있었으며, 다핵거대세포가 출현하였다. 사이질조직의 부종은 관찰할 수 없었으며, 사이질세포 역시 비교적 온전하게 보존되어 있었다. 따라서 6-AN은 햄스터 정소에서 정자발생세포, 지지세포 등에는 영향을 미치나 사이질세포에는 영향을 주지 않는 것으로 사료된다.

• Animal cells and systems
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• 제9권4호
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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.

• 한국동물학회:학술대회논문집
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• 한국동물학회 2003년도 한국생물과학협회 학술발표대회
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• pp.170.1-170
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• 2003

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 2001년도 공동 춘계학술대회
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• pp.30-31
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• 2001

No Abstract, See Full Text