[ABSTRAK Proliferasi sel merupakan peningkatan dalam jumlah sel sebagai hasil daripertumbuhan dan pembelahan sel. Selain terjadi pada sel normal pembelahan seljuga terjadi pada sel kanker yang ditandai dengan proliferasi tak terkendali.Banyak di antara penghambatan proliferasi dilakukan dengan cara menghambatsintesis DNA, yaitu mengintervensi pembentukan basa nukleotida purin ataupirimidin. Mengingat dalam sintesis purin de novo terdapat peran biotin yangmerupakan koenzim dalam proses karboksilasi, maka penambahan avidin didugakuat dapat mengikat biotin dengan afinitas yang sangat tinggi. Penelitian inibertujuan untuk mempelajari potensi avidin dalam kemampuannya mengikat botinuntuk menghambat mitosis. Pada penelitian ini SMDT dikultur dalam mediumyang distimulasi oleh PHA, IL-2, serta PHA dan IL-2 dengan dan tanpa avidin.Efek dari penambahan avidin ini dilihat pada jam-jam tertentu dan dilakukananalisis terhadap proliferasi, viabilitas, serta siklus sel. Berdasarkan hasilpenelitian, avidin menghambat proliferasi SMDT serta menurunkan viabilitasSMDT baik pada kultur yang distimulasi PHA maupun pada kultur yangdistimulasi PHA dan IL-2. Penambahan avidin juga menghambat masuknyaprogresi SMDT yang dikultur selama 72 jam dari fase G0/G1 ke fase S. Penelitianini menunjukkan bahwa avidin dapat mengikat biotin yang ada dalam mediumsehingga proliferasi sel menjadi terhambat. ABSTRACT Cell proliferation is the increment of cell number as a result of cell growth andcell division. Cell division occurs not only in normal cells but also in cancer cellswhich undergo uncontrolled cell division. Most of the cell proliferation inhibitionwas done by inhibiting the DNA synthesis by which intervening the formation ofpurine or pyrimidine nucleotide bases. Considering the role of biotin in purine denovo synthesis as a coenzyme in the carboxylation reaction, it was assumed thatavidin can bind biotin with very high affinity. The aim of this research is to studythe potential of avidin to bind biotin for inhibit mitosis. In this study PBMC wascultured in a medium that stimulated by PHA, IL-2, PHA and IL-2 with andwithout avidin. The effect of the addition of avidin was observed at certain hoursfor the analysis of proliferation, viability, and cell cycle. This study suggest thatavidin inhibits proliferation and decreases viability of PBMC both of PBMCstimulated by PHA and stimulated by PHA and IL-2. The addition of avidin alsoinhibits the entry of progression of PBMC when cultured for 72 hours from phaseG0/G1 to S phase. Based on these data, we propose that avidin might bindextracellular biotin in the medium therefore the cell proliferation was inhibited;Cell proliferation is the increment of cell number as a result of cell growth andcell division. Cell division occurs not only in normal cells but also in cancer cellswhich undergo uncontrolled cell division. Most of the cell proliferation inhibitionwas done by inhibiting the DNA synthesis by which intervening the formation ofpurine or pyrimidine nucleotide bases. Considering the role of biotin in purine denovo synthesis as a coenzyme in the carboxylation reaction, it was assumed thatavidin can bind biotin with very high affinity. The aim of this research is to studythe potential of avidin to bind biotin for inhibit mitosis. In this study PBMC wascultured in a medium that stimulated by PHA, IL-2, PHA and IL-2 with andwithout avidin. The effect of the addition of avidin was observed at certain hoursfor the analysis of proliferation, viability, and cell cycle. This study suggest thatavidin inhibits proliferation and decreases viability of PBMC both of PBMCstimulated by PHA and stimulated by PHA and IL-2. The addition of avidin alsoinhibits the entry of progression of PBMC when cultured for 72 hours from phaseG0/G1 to S phase. Based on these data, we propose that avidin might bindextracellular biotin in the medium therefore the cell proliferation was inhibited, Cell proliferation is the increment of cell number as a result of cell growth andcell division. Cell division occurs not only in normal cells but also in cancer cellswhich undergo uncontrolled cell division. Most of the cell proliferation inhibitionwas done by inhibiting the DNA synthesis by which intervening the formation ofpurine or pyrimidine nucleotide bases. Considering the role of biotin in purine denovo synthesis as a coenzyme in the carboxylation reaction, it was assumed thatavidin can bind biotin with very high affinity. The aim of this research is to studythe potential of avidin to bind biotin for inhibit mitosis. In this study PBMC wascultured in a medium that stimulated by PHA, IL-2, PHA and IL-2 with andwithout avidin. The effect of the addition of avidin was observed at certain hoursfor the analysis of proliferation, viability, and cell cycle. This study suggest thatavidin inhibits proliferation and decreases viability of PBMC both of PBMCstimulated by PHA and stimulated by PHA and IL-2. The addition of avidin alsoinhibits the entry of progression of PBMC when cultured for 72 hours from phaseG0/G1 to S phase. Based on these data, we propose that avidin might bindextracellular biotin in the medium therefore the cell proliferation was inhibited] |