• 제목/요약/키워드: polyamines

검색결과 148건 처리시간 0.038초

Dexamethasone에 의한 생쥐 흉선의 Apoptosis에서 Polyamine의 역할 (Inhibitory Role of Polyamines in Dexamethasone-induced Apoptosis of Mouse Thymocytes)

  • 최상현;김용훈;홍기현;신경호;천연숙;전보권
    • 대한약리학회지
    • /
    • 제32권1호
    • /
    • pp.113-123
    • /
    • 1996

  • 세포내 polyamine은 DNA 구조 뿐 아니라 전사과정, 세포의 성장, 분화, 및 증식 등에 간여하는 바, 배양 흉선세포의 apoptosis 을 억제한다고 한다. 따라서 dexamethasone에 의한 생쥐 흉선세포의 apoptosis 반응에 대한 polyamine의 억제작용을, polyamine 생성과 대사억제제들로 처치한 흉선세포의 일차배양실험에서 관찰하여, 그 결과를 A23187과 DHEA의 작용과 비교하였다. 1) 흉선세포 생존율이 dexamethasone, DHEA, A23187, DFMO, MGBG들에 의하여 직접 현저히 억제되며, aminoguanidine, putrescine, spermidine, 및 spermine들에 의해서는 영향을 받지 않았다. 2) 흉선세포 DNA의 분절화가 dexamethasone과 A2318T에 의하여 유의하게 증강되어 있으며 DHEA에 의하여도 다소 증가되었으나, DFMO, MGBG, aminoguanidine, putrescine, spermidine, 및 spermine들에 의하여는 크게 영향을 받지 않았다. 3) Dexamethasone에 의한 흉선세포의 apoptosis는 DHEA에 의하여 억제된 반면, DFMO, MGBG, 및 aminoguanidine에 의하여는 영향을 받지 않았다. Spermine은 dexamethasone과 A23187에 의한 세포생존율 감소를 유의하게 억제하였으며, A23187에 의한 세포생존율 감소는 putrescine과 spermidine에 의하여도 억제되는 경향을 보였다. 4) DFMO 및 MGBG에 의한 흉선세포 생존율 감소는 spermine에 의해 현저히 억제되었으나, putrescine과 spermidine에 의하여는 영향을 받지 않았다. 5) Dexamethasone을 DFMO 또는 MGBG와 병합처치하여 나타나는 흉선세포 생존율 감소는 각각 spermine과 putrescine에 의하여 유의하게 억제되었으나, aminoguanidine 또는 DHEA와 dexamethasone의 병합처치에 의한 생존율 감소는 polyamine 전처치에 의해 감소되지 않았다. 이상의 결과는 polyamine이 흉선세포의 apoptosis 반응을 억제할 수 있고, 이같은 억제효과의일부가 $[Ca^{2+}]_i$ 증가에 관련되는 신호전달과정과 연관될 뿐 아니라, 세포막의 polyamine transporter를 통한 polyamine 섭취가 이들의 생합성 또는 유리기능과 함께 세포내 polyamine 함량을 조정하므로, 흉선세포의 apoptosis에 억제적으로 작용할 수 있음을 시사하는 것으로 사료된다.

  • PDF

Effects of Agmatine on Polyamine Metabolism and the Growth of Prostate Tumor Cells

  • Choi, Yon-Sik;Cho, Young-Dong
    • BMB Reports
    • /
    • 제32권2호
    • /
    • pp.173-180
    • /
    • 1999

  • The effects of agmatine on the enzymes responsible for the biosynthesis of polyamines, the resultant levels of polyamines, and their effect on the growth of DU145 human prostate tumor cells were investigated. When agmatine was added to the medium, ornithine decarboxylase (ODC, EC 4.1.1.17) activity was substantially reduced, but S-adenosylmethionine decarboxylase (SAMDC, EC 4.1.1.50) activity increased markedly. These changes in ODC and SAMDC activities were the result of an induction of ODC-antizyme and a decreased turnover rate of SAMDC in the presence of agmatine. Accordingly, there was a decrease in the intracellular levels of putrescine and spermidine but an increase in the intracellular level of spermine. Cell growth was markedly inhibited by agmatine treatment and this inhibition was not recovered by the addition of putrescine or spermidine. Our results suggest that agmatine alters the intracellular amounts of polyamine in the cells, closely related to the inhibition of cell growth.

  • PDF

Kinetic Analyses of Spermine Effects on Petiole Elongation in Ranunculus sceleratus

  • Chang, Soo-Chul
    • Journal of Plant Biology
    • /
    • 제37권4호
    • /
    • pp.397-402
    • /
    • 1994

  • Possible roles of polyamines in the inhibition of cell elongation in Ranunculus petioles were investigated. Exogenously apoplied polyamines greatly inhibited the auxin-induced petiole growth, while treatment of the tissue with $\alpha$-difluoromethylarginine, the inhibitor of putrescine biosynthesis, further enhanced the growth in the presence of IAA. Inhibitory effect of spermine can also be apparent for fusicoccin-induced elongation, but not for growth induced by a low pH. Spermine also suppressed the ethylene-enhanced growth in the presence of auxin. Using computer-based video digitizer system, the inhibitory effects of spermine on petiole growth were kinetically analyzed. Auxin-induced growth was characterized by an initial and transient growth with a highly elevated rate followed by a steady growth with a slightly reduced rate. Spermine treatment was found to shorten the duration of the initial phase of growth, and to reduce the rates of both the initial and steady growth as well. The latent period for auxin induction was not affected by spermine.

  • PDF