Nutrition & Food Science
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Item EFFECT OF CHITOSAN ON THE INDUCTION OF DNA DAMAGE RESPONSE BY SELENIUM COMPOUNDS.(2009) Zhang, Shu; Cheng, Wen-Hsing; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)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 efficacy of Se in mitigating tumorigenesis. We applied Se compounds, which is from sub-lethal to lethal dose, to colon cancer cell line HCT-116 and normal fibroblasts cell line MRC-5. Analysis of cellular selenium content demonstrated that: 1) Na2SeO3, but not MSeA, treatment resulted in a greater Se retention in HCT-116 than in MRC-5 cells, 2) chitosan encapsulation enhanced Se contents in cells treated with the various Se preparations. Cell survival analysis showed that chitosan encapsulation protected HCT-116 and MRC-5 cells from Na2SeO3 or MSeA induced toxicity. Moreover, this beneficial effect was greater in MRC-5 cells. MSeA encapsulated with chitosan induced phosphorylated ATM Ser-1981 formation in MRC-5 and HCT-116 cells to a less extent as compared to MSeA alone treatment. 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.Item THE FUNCTION OF MRN (MRE11-RAD50-NBS1) COMPLEX DURING WRN (WERNER) FACILITATED ATM (ATAXIA-TELANGIECTASIA MUTATED) ACTIVATION(2009) Ma, Junhao; Cheng, Wen-Hsing; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)WRN (Werner) protein is a member of the RecQ family showing helicase and exonuclease activity. WRN protein may lose function upon mutation and causes Werner syndrome (WS) which is an autosomal recessive, cancer-prone and premature aging disease. ATM (Ataxia-Telangiectasia mutated) protein initiates a signaling pathway in response to DNA double strand breaks (DSBs). Genomic disorder ataxia-telangiectasia (A-T) is associated with defective ATM. WRN protein is involved in ATM pathway activation when cells are exposed to DSBs associated with replication fork collapse. Because the Mre11-Rad50-Nbs1 (MRN) complex, a sensor of DSBs, is known to interact with WRN and ATM, we investigated whether the MRN complex mediates the WRN-dependent ATM pathway activation. In this study, we employed short-hairpin RNA to generate WRN- and Nbs1-deficient U-2 OS (osteosarcoma) cells. Cells were treated with clastogens which induce collapsed replication forks, thus provided proof for whether WRN facilitates ATM activation via MRN complex. This study serves as a basis for future investigation on the correlation between ATM, MRN complex and WRN, which will ultimately help understand the mechanism of aging and cancer.Item THE EFFECTS OF OBESITY ON PLASMA LEVELS OF OMENTIN, A DEPOT-SPECIFIC ADIPOCYTOKINE(2004-08-27) de Souza Batista, Celia Maria; Kantor, Mark; McLenithan, John; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Obesity is a chronic pathological condition and a risk factor for diabetes and cardiovascular disease. It has been demonstrated that adipose tissue functions not only as a fat storage depot but also as an endocrine organ. Omentin is a protein expressed and secreted in adipose tissue that increases insulin-stimulated glucose transport. To further elucidate omentin's physiological function, its levels were measured by quantitative western blotting in plasma from 44 healthy nondiabetic volunteers (22 women, 22 men). Participants were organized into sibling pairs based on discordant BMI (3-12 Kg/m2). Lean subjects had significantly higher omentin levels than obese/overweight subjects (independent of sex), and significantly higher omentin levels were detected in women compared to men. Omentin levels were inversely correlated with BMI and positively correlated with HDL levels. These data suggest that omentin may play a physiological role in the pathogenesis of obesity-dependent insulin resistance.