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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2016.4
- 수록면
- 72 - 79 (8page)
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초록· 키워드
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Purpose: The initiation of mandatory folic acid fortification using pteroylmonoglutamic acid (PteGlu) has reduced the rate of congenital malformations. However, it also appears to be responsible for several adverse effects, including increased cancer incidence. This may be related to physicho-chemical characteristics of PteGlu. This study examines the potential effect of high concentrations of PteGlu on a population subjected to mandatory folic acid fortification using an in vitro model. Methods: Caco-2 (colorectal cancer) and MCF7 (breast cancer) cell lines were cultured at 6 different PteGlu concentrations (0, 0.1, 1, 50, 250, and 500μg/ml) for 6 days. Cell growth was determined using thiazolyl blue tetrazolium bromide assay. The genotype of dihydrofolate reductase 19bp deletion/insertion (DHFR 19-del) was also scored in cell lines using a restriction fragment length polymorphism technique to examine whether genetic variations may factor in cell proliferation. Results: PteGlu exhibited differential growth promoting properties between cell lines. Caco-2 cells did not show a significant growth difference at low concentrations compared to control, however, at higher concentrations, the growth showed a contrasting trend in the early experimental period, while MCF7 showed enhanced cell growth at all concentrations. The DHFR 19-del genotype differed in the two cell lines. Conclusions: Altered response to PteGlu by Caco-2 and MCF7 may reflect a tissue specific disease aetiology or genotype specific differential enzyme activity, for example by DHFR, to critical levels of PteGlu. As folic acid fortification is a blanket intervention, and DHFR and other enzyme activities vary between individuals, PteGlu intake may have an as yet undefined effect on health. These findings may be relevant when considering mandatory folic acid fortification for disease prevention.
목차
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
CONCLUSION
REFERENCES
참고문헌 (44)
참고문헌 신청
Prinz-Langenohl R, Fohr I, Pietrzik K. Beneficial role for folate in the prevention of colorectal and breast cancer. Eur J Nutr 2001; 40(3): 98-105.
Kim YI. Folate and colorectal cancer: an evidence-based critical review. Mol Nutr Food Res 2007; 51(3): 267-292.
Kim YI. Role of folate in colon cancer development and progression. J Nutr 2003; 133(11 Suppl 1): 3731S-3739S.
Kim YI. Folate and carcinogenesis: evidence, mechanisms, and implications. J Nutr Biochem 1999; 10(2): 66-88.
Choi SW, Mason JB. Folate status: effects on pathways of colorectal carcinogenesis. J Nutr 2002; 132(8 Suppl): 2413S-2418S.
Kim YI. Folate and colorectal cancer: an evidence-based critical review. Mol Nutr Food Res 2007; 51(3): 267-292.
Kim YI. Role of folate in colon cancer development and progression. J Nutr 2003; 133(11 Suppl 1): 3731S-3739S.
Kim YI. Folate and carcinogenesis: evidence, mechanisms, and implications. J Nutr Biochem 1999; 10(2): 66-88.
Choi SW, Mason JB. Folate status: effects on pathways of colorectal carcinogenesis. J Nutr 2002; 132(8 Suppl): 2413S-2418S.
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UCI(KEPA) : I410-ECN-0101-2016-594-002844104