This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Connelly, A. E. Articles by Sandler, R. S. Search for Related Content PubMed PubMed Citation Articles by Connelly, A. E. Articles by Sandler, R. S.

Vitamin C Intake and Apoptosis in Normal Rectal Epithelium¹

Departments of Epidemiology [A. E. C., C. F. M., R. S. S.], Nutrition [J. S-A.], Medicine [C. F. M., T. O. K., R. S. S.], Pathology [J. T. W.], and Molecular and Cellular Physiology [P. K. L.], University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7555

Apoptosis, or programmed cell death, may lower the risk of neoplasia by removing genetically damaged or mutated cells. A high rate of apoptosis has been linked to a reduced risk of colorectal adenomas; therefore, it is important to understand factors that impact apoptosis. Antioxidants (e.g., vitamin C) protect cells from harmful oxidation processes but may interfere with apoptosis by protecting genetically damaged cells from reactive oxygen species-dependent cell death. The objective of this study was to evaluate the association between vitamin C intake and apoptosis in normal rectal mucosa. Study participants were part of a large, cross-sectional study, the Diet and Health Study III. Participants were recruited from consecutive, consenting patients who underwent colonoscopy at University of North Carolina Hospitals between August 1, 1998 and March 4, 2000. Vitamin C intake, obtained from a food frequency questionnaire, included both dietary sources and vitamin supplements. Apoptosis was measured by morphological evaluation of H&E-stained sections obtained from pinch biopsy samples of normal rectal mucosa in consenting participants (n = 503). The relationship between vitamin C and apoptosis varied by adenoma status. Among individuals with adenomas, there was an inverse linear association between apoptosis and total vitamin C intake. Similarly, individuals with adenomas in the highest quintile of total vitamin C intake were substantially less likely than those in the lowest quintile to have increased colonic apoptosis (odds ratio, 0.05; 95% confidence interval, 0.01–0.46). Vitamin C was not significantly associated with apoptosis in adenoma-free patients. High vitamin C intake was associated with reduced colorectal apoptosis among individuals with adenomas in this study population. Given that high apoptosis may lower colorectal cancer risk, vitamin C supplements may be contraindicated for patients with a history of adenomas.

This article has been cited by other articles:

				T. O. Keku, A. Amin, J. Galanko, C. Martin, B. Schliebe, and R. S. Sandler Apoptosis in Normal Rectal Mucosa, Baseline Adenoma Characteristics, and Risk of Future Adenomas Cancer Epidemiol. Biomarkers Prev., February 1, 2008; 17(2): 306 - 310. [Abstract] [Full Text] [PDF]

				M. C. Stern, K. D. Siegmund, R. Corral, and R. W. Haile XRCC1 and XRCC3 Polymorphisms and Their Role as Effect Modifiers of Unsaturated Fatty Acids and Antioxidant Intake on Colorectal Adenomas Risk Cancer Epidemiol. Biomarkers Prev., March 1, 2005; 14(3): 609 - 615. [Abstract] [Full Text] [PDF]

				E. A. Miller, T. O. Keku, J. A. Satia, C. F. Martin, J. A. Galanko, and R. S. Sandler Calcium, Vitamin D, and Apoptosis in the Rectal Epithelium Cancer Epidemiol. Biomarkers Prev., February 1, 2005; 14(2): 525 - 528. [Abstract] [Full Text] [PDF]

				U. Wenzel, A. Nickel, S. Kuntz, and H. Daniel Ascorbic acid suppresses drug-induced apoptosis in human colon cancer cells by scavenging mitochondrial superoxide anions Carcinogenesis, May 1, 2004; 25(5): 703 - 712. [Abstract] [Full Text] [PDF]

				C. D. Albright, R. I. Salganik, and T. Van Dyke Dietary Depletion of Vitamin E and Vitamin A Inhibits Mammary Tumor Growth and Metastasis in Transgenic Mice J. Nutr., May 1, 2004; 134(5): 1139 - 1144. [Abstract] [Full Text] [PDF]