Low LET X-ray가 췌장β세포와 신경세포에 미치는 효과 = Effect on Pancreatic Beta Cells and Nerve Cells by Low LET X-ray

국문 초록 (Abstract)

배양된 췌장베타세포와 신경세포를 10% FBS(fetal bovine serum), 11.1 mM glucose의 normal 조건과 1% FBS, 30 mM glucose의 hyperglycemia 조건으로 배양하고, 저 LET X-tjs을 0.5 Gy/hr의 선량률로 총 선량이 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 5 Gy가 되도록 저 LET 방사선을 조사한 후 MTT assay로 생존율을 측정하고 비교하였다.
분화된 췌장베타세포에 방사선을 조사하지 않았을 때는 normal 조건에 비해 hyperglycemia 조건의 생존율이 경미한 감소를 보였다. 그러나 X선의 총 선량이 점차 누적됨에 띠라 normal 조건에서 생존율이 조금씩 감소하는 것에 비해 hyperglycemia 조건에서는 급격히 감소하여 시너지 효과를 나타냈다.
미분화된 신경세포에서는 방사선을 조사하지 않은 때도 normal 조건에 비해 hyperglycemia 조건의 생존율이 뚜렷하게 감소하였다. X선의 총 선량이 점차 누적됨에 따라 normal 과 hyperglycemia 조건 모두에서 비교적 급격한 세포사멸이 나타났지만 그 생존율의 감소비율이 거의 평행하게 진행되어 시너지 효과를 보이지 않았다.

다국어 초록 (Multilingual Abstract)

Cultured pancreatic beta cells and nerve cells, it is given normal condition of 10% FBS (fetal bovine serum), 11.1 mM glucose and hyperglycemia codition of 1% FBS, 30 mM glucose. For low LET X-ray irradiated with 0.5 Gy/hr dose-rate(total dose: 0.5 to 5 Gy). Survival rates were measured by MIT assay.
When non irradiated, differentiated in the pancreatic beta cells experiment is hyperglycemia conditions survival rate compared to normal conditions survival rate seemed a small reduction. However increasing the total dose of X-ray, the survival rate of normal conditions decreased slightly compared to the survival rate of hyperglycemia conditions, the synergistic effect was drastically reduced.
When non irradiated, undifferentiated in the nerve cells experiment is hyperglycemia conditions survival rate compared to normal conditions survival rate seemed a large reduction. As the cumulative dose of X-ray normal conditions and hyperglycemia were all relatively rapid cell death. But the rate of decreased survivals by almost parallel to the reduction proceed and it didn't show synergistic effect.

목차 (Table of Contents)

• 국문초록
• Ⅰ. 서론
• Ⅱ. 연구 방법
• Ⅲ. 연구 결과
• Ⅳ. 고찰 및 결론
• 참고문헌
• Abstract

참고문헌 (Reference)

1 Liu SZ., "Thymocyte apoptosis in response to low-dose radiation" 175-358, 1996

2 Jeong-Won Im, "The relevance of diabetes management of the amount of stress associated with life events in diabetic patients" 25 (25): 240-247, 2001

3 Bo-Ra Im, "Pancreatic beta cells to GLP-1's Glucosamine by toxicity protection mechanisms" Gye-myeong University 2007

4 Elisabetta babetto, AM, "MR : tetracycline-regulated gene expression in the NSC-34-tTA cell line for investigation of motor neuron disease" 140 : 63-72, 2005

5 Prasad AV., "Induction of "immediate early genes" by Low dose loruzlng radiation" 143-263, 1995

6 Marshak S, "Impaired beta-cell functions induced by chronic exposure of cultured human pancreatic islets to high glucose" 48 (48): 1230-1236, 1999

7 Donath MY, "Hyperglycemia-induced beta-cell apoptosis in pancreatic islets of Psammomys obesus during development of diabetes" 48 (48): 738-744, 1999

8 Keun-Gyu Park, "Glucotoxicity in the INS-1 Rat Insulinoma Cell Line Is Mediated by theOrphan Nuclear Receptor Small Heterodimer Partner" 56 : 2007

9 Efanova IB, "Glucose and tolbutamide induce apoptosis in pancreatic beta-cells. A process dependent on intracellular Ca2+Ca2+ concentration" 273 (273): 33501-33507, 1998

10 Seigou Usuki, "GM2 Promotes ciliary Neurotrophic Factor-Dependent Rescue of Immortalized Motor Neuron-Like Cell(NSC-34)" 24 (24): 281-286, 1999

11 Feinendegen, LE., "Biochemical and cellular mechanisms of low-dose effects" 23-53, 1988

12 Yan Yang, "A highly Ca2+Ca2+-sensitive Pool of Granules Is Regulated by Glucose and Protein Kinases in Insulin-secreting INS-1 Cells"

13 Kyu Chang Won, "A Protective Role for Heme Oxygenase-1 in INS-1 Cells and Rat Islets that are Exposed to High Glucose Conditions" 대한의학회 21 (21): 418-424, 2006