Background: Hypertension is a pathological increase in blood pressure that affects nearly 30% of the U.S. population and is a primary modifiable risk factor for cardiovascular disease. Despite advancements in prevention and treatment, hypertension is still one of the most common conditions around the world, and for a majority of cases the causal mechanisms remain to be fully elucidated. A growing body of literature suggests that oxidative stress status may play an etiological role in many chronic conditions, including hypertension. Specifically, a systemic overabundance of reactive oxygen species may give rise to endothelial dysfunction, increased sodium and H2O retention, and alterations in sympathetic outflow, leading to an increase in blood pressure. Purpose: The main objective of this study is to investigate the prospective association between F2-isoprostanes, a validated biomarker of oxidative status, and development of hypertension in a large, multi-centered, multi-ethnic cohort of adults aged 40-69 at baseline. Methods: This is a secondary data analysis that utilized previously collected data from the Insulin Resistance Atherosclerosis Study. 844 participants were included in the analysis. Briefly, four urinary F2-isoprostane isomers (F2-IsoP1, F2-IsoP2, F2-IsoP3, and F2-IsoP4) were quantified using liquid chromatography/ tandem mass spectrometry and adjusted for urinary creatinine levels. Hypertension was assessed at baseline and follow-up visits and defined as systolic blood pressure > 140 mm Hg and/or diastolic blood pressure > 90 mm Hg and/or currently taking antihypertensive medications. Crude associations between study population characteristics and hypertensive status were analyzed with the chi-square and Wilcoxon-rank sum tests. Crude associations between study population characteristics and F2-isoprostane levels were analyzed with Wilcoxon-rank sum, Kruskal-Wallis, and Spearman’s rank correlation measures. Finally, the adjusted prospective associations between hypertensive status and F2-isoprostane concentrations were modeled using logistic regression. Results: Of the 844 participants who were included in the study, 258 (31%) were classified as hypertensive at baseline. Among the 586 participants who were normotensive at baseline, 123 (21%) developed hypertension over the five-year study period. Importantly, none of four F2-isoprostane isomers predicted a significant increase in the odds of developing hypertension, as indicated by their odds ratio 95% confidence intervals; F2-IsoP1: (0.85, 1.31), F2-IsoP2: (0.62, 1.13), F2-IsoP3: (0.80, 1.27), and F2-IsoP4: (0.84, 1.29). Conclusion: Previous studies have investigated the association between oxidative status and hypertension prevalence, however the cross sectional nature of the study designs have made it difficult to establish temporality between exposure and outcome. To our knowledge, this is the first study to model the odds of developing hypertension as a function of F2-isoprostane levels. The results of this study suggest that oxidative status is not involved in the development of hypertension.

Red raspberries, as an excellent source of dietary antioxidants, were investigated for their effect on oxidative stress in healthy adults. Study 1 measured effects of chronic exposure in a parallel, multi-dose intervention. Subjects consumed one-cup red raspberries (1cR) daily for two-weeks, then were randomized to consume 1cR, 2cR or 4cR for additional two-weeks (n=8, by group). There was a reduction in TBARS, indicating a decrease in lipid peroxidation, after two-weeks of intervention in the 1cR group, but effects were not significant at week 4, or for other treatment groups. Study 2 measured effects of acute exposure using a cross-over design. Subjects (n=8) consumed single treatments of 1cR, 2cR, 4cR, bread and bread plus vitamin C. Post-prandial oxidative stress responses were complex and appeared related to calorie and antioxidant load. Overall there was no clear relationship between red raspberry consumption and protection against oxidative stress.

Thesis (M.S.)--Auburn University, 2007. / Abstract. Vita. Includes bibliographic references (ℓ. 90-99)

Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 4 uppsatser.

Thesis (M.S.)--West Virginia University, 2007. / Title from document title page. Document formatted into pages; contains vii, 51 p. : ill. Includes abstract. Includes bibliographical references.

Thesis (Ph.D.)--University of Wisconsin--Madison, 2006. / Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D.)--University of Missouri--Rolla, 2007. / Vita. The entire thesis text is included in file. Title from title screen of thesis/dissertation PDF file (viewed January 28, 2008) Includes bibliographical references (p. 117-131).

Thesis (Ph.D.)--Auburn University, 2007. / Abstract. Vita. Includes bibliographic references (ℓ. 115-137)

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2002. / Härtill 5 uppsatser.