oxidative stress is caused by an imbalance between the production and removal of reactive oxygen species (ros). polyunsaturated fatty acids (pufa), due to their multiple carbon-carbon double bonds, react readily with ros in a process termed lipid peroxidation. lipid peroxidation generates a number of potentially harmful secondary products, including the aldehydes ethanal, propanal, and hexanal. indeed, raised aldehyde levels have been associated with various diseases, including cancer, leading researchers to consider them as potential diagnostic markers. however the abundance of their fatty acid precursors is dependent on dietary intake. as such, tissue aldehyde content may be diet-dependent, reducing their desirability as markers. to investigate this i fed 32 male wistar rats diets containing 90% fat-free rat chow, 9% palm oil (mostly saturated fat), and 1% omega-3 fatty acid (epa, dha, ala) for 8 weeks. the different diets resulted in changed fatty acid lipid composition in rat brain and liver. compared to controls, dha and epa diets decreased liver arachidonic acid levels by 10%, while increasing levels of epa and dha by 7-11%. a similar effect was seen in brain lipid composition, although the changes, while statistically significant, weren’t as pronounced. in brain lipids, feeding omega-3 pufa did not lead to great changes in their concentrations, while dha was found to be maintained at high levels even in the absence of any omega-3 pufa in the diet. however, selected ion flow mass-spectrometry (sift-ms) analysis of the rat livers and brains suggests that diet does not significantly affect the concentrations of various aldehydes (p>0.05), or overall levels of oxidative stress (as measured by tbars assays) in liver or brain (p>0.05). my results suggest that volatile aldehydes may represent a useful marker for oxidative stress with potential applications in a variety of common disorders.