[
ABSTRAKProliferasi sel merupakan peningkatan dalam jumlah sel sebagai hasil dari
pertumbuhan dan pembelahan sel. Selain terjadi pada sel normal pembelahan sel
juga terjadi pada sel kanker yang ditandai dengan proliferasi tak terkendali.
Banyak di antara penghambatan proliferasi dilakukan dengan cara menghambat
sintesis DNA, yaitu mengintervensi pembentukan basa nukleotida purin atau
pirimidin. Mengingat dalam sintesis purin de novo terdapat peran biotin yang
merupakan koenzim dalam proses karboksilasi, maka penambahan avidin diduga
kuat dapat mengikat biotin dengan afinitas yang sangat tinggi. Penelitian ini
bertujuan untuk mempelajari potensi avidin dalam kemampuannya mengikat botin
untuk menghambat mitosis. Pada penelitian ini SMDT dikultur dalam medium
yang 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 dilakukan
analisis terhadap proliferasi, viabilitas, serta siklus sel. Berdasarkan hasil
penelitian, avidin menghambat proliferasi SMDT serta menurunkan viabilitas
SMDT baik pada kultur yang distimulasi PHA maupun pada kultur yang
distimulasi PHA dan IL-2. Penambahan avidin juga menghambat masuknya
progresi SMDT yang dikultur selama 72 jam dari fase G0/G1 ke fase S. Penelitian
ini menunjukkan bahwa avidin dapat mengikat biotin yang ada dalam medium
sehingga proliferasi sel menjadi terhambat.
ABSTRACTCell proliferation is the increment of cell number as a result of cell growth and
cell division. Cell division occurs not only in normal cells but also in cancer cells
which undergo uncontrolled cell division. Most of the cell proliferation inhibition
was done by inhibiting the DNA synthesis by which intervening the formation of
purine or pyrimidine nucleotide bases. Considering the role of biotin in purine de
novo synthesis as a coenzyme in the carboxylation reaction, it was assumed that
avidin can bind biotin with very high affinity. The aim of this research is to study
the potential of avidin to bind biotin for inhibit mitosis. In this study PBMC was
cultured in a medium that stimulated by PHA, IL-2, PHA and IL-2 with and
without avidin. The effect of the addition of avidin was observed at certain hours
for the analysis of proliferation, viability, and cell cycle. This study suggest that
avidin inhibits proliferation and decreases viability of PBMC both of PBMC
stimulated by PHA and stimulated by PHA and IL-2. The addition of avidin also
inhibits the entry of progression of PBMC when cultured for 72 hours from phase
G0/G1 to S phase. Based on these data, we propose that avidin might bind
extracellular biotin in the medium therefore the cell proliferation was inhibited;Cell proliferation is the increment of cell number as a result of cell growth and
cell division. Cell division occurs not only in normal cells but also in cancer cells
which undergo uncontrolled cell division. Most of the cell proliferation inhibition
was done by inhibiting the DNA synthesis by which intervening the formation of
purine or pyrimidine nucleotide bases. Considering the role of biotin in purine de
novo synthesis as a coenzyme in the carboxylation reaction, it was assumed that
avidin can bind biotin with very high affinity. The aim of this research is to study
the potential of avidin to bind biotin for inhibit mitosis. In this study PBMC was
cultured in a medium that stimulated by PHA, IL-2, PHA and IL-2 with and
without avidin. The effect of the addition of avidin was observed at certain hours
for the analysis of proliferation, viability, and cell cycle. This study suggest that
avidin inhibits proliferation and decreases viability of PBMC both of PBMC
stimulated by PHA and stimulated by PHA and IL-2. The addition of avidin also
inhibits the entry of progression of PBMC when cultured for 72 hours from phase
G0/G1 to S phase. Based on these data, we propose that avidin might bind
extracellular biotin in the medium therefore the cell proliferation was inhibited, Cell proliferation is the increment of cell number as a result of cell growth and
cell division. Cell division occurs not only in normal cells but also in cancer cells
which undergo uncontrolled cell division. Most of the cell proliferation inhibition
was done by inhibiting the DNA synthesis by which intervening the formation of
purine or pyrimidine nucleotide bases. Considering the role of biotin in purine de
novo synthesis as a coenzyme in the carboxylation reaction, it was assumed that
avidin can bind biotin with very high affinity. The aim of this research is to study
the potential of avidin to bind biotin for inhibit mitosis. In this study PBMC was
cultured in a medium that stimulated by PHA, IL-2, PHA and IL-2 with and
without avidin. The effect of the addition of avidin was observed at certain hours
for the analysis of proliferation, viability, and cell cycle. This study suggest that
avidin inhibits proliferation and decreases viability of PBMC both of PBMC
stimulated by PHA and stimulated by PHA and IL-2. The addition of avidin also
inhibits the entry of progression of PBMC when cultured for 72 hours from phase
G0/G1 to S phase. Based on these data, we propose that avidin might bind
extracellular biotin in the medium therefore the cell proliferation was inhibited]
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