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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #251436

Title: Effect of Chitosan on the Induction of DNA Damage Response by Selenium Compounds

item ZHANG, SHU - University Of Maryland
item Zeng, Huawei
item LUO, YANGCHAO - University Of Maryland
item WANG, QIN - University Of Maryland
item CHENG, WEN-HSING - University Of Maryland

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/15/2009
Publication Date: 4/24/2010
Citation: Zhang, S., Zeng, H., Luo, Y., Wang, Q., Cheng, W. 2010. Effect of Chitosan on the Induction of DNA Damage Response by Selenium Compounds. Journal of Federation of American Societies for Experimental Biology. 24:lb251.

Interpretive Summary:

Technical Abstract: Selenium (Se), a nutrient trace mineral, plays important roles in optimizing human health. Chitosan is an effective, natural-oriented material for synthesizing nanopolymers, with preferable properties such as biocompatibility, biodegradation and resistance to certain enzymes. In this study, encapsulated Na2SeO3 and methylseleninic acid (MSeA) with low and medium molecular weight chitosan were used to determine the effect of chitosan on Se-induced DNA damage response. We applied a range of Se compounds to the HCT 116 colon cancer cell line and the MRC-5 normal fibroblasts. Analysis of cellular Se content demonstrated that: 1) cellular Se retention is greater in HCT-116 than in MRC-5 cells, 2) chitosan encapsulation enhanced Se contents in both the cells. Cell survival analysis showed that chitosan encapsulation protects against Na2SeO3 or MSeA induced cell killing, and the extent of which is more pronounced in MRC-5 than in HCT 116 cells. Chitosan encapsulation decreases Se-induced ATM phosphorylation Ser-1981 in both MRC-5 and HCT-116 cells. Taken together, the results suggest that, when encapsulated with chitosan, cells are less susceptible to Se treatment, possibly through a mechanism by which the presence of chitosan attenuates Se-induced activation of ATM and corresponding DNA damage response pathway.