Nutritional level and energetic source are determinants of elevated circulatory lipohydroperoxide concentration.

Dietary energetic impact on oxidative stress is incompletely understood. Therefore, effects of diets on oxidative stress were studied using a crossover block design. In Expt 1, intake of metabolizable energy (ME) was restricted or ad libitum. In Expt 2, isoenergetic and isonitrogenic diets were fed, replacing carbohydrate energy by energy of fatty acids. Circulatory lipohydroperoxides (LOOH), markers of acute oxidative stress, were expressed absolutely and in terms of cholesterol or TAG levels. In Expt 1, plasma (jugularis vein) LOOH was assayed in combination with whole-body oxidative metabolism using gas exchange and heart rate (HR) during feeding periods and at rest. In Expt 2, LOOH was assayed in plasma from portal and a large udder vein and a mesenteric artery. In Expt 1, intake increased VO2, HR and LOOH following overnight fast with higher values (P < 0.05) when feeding ME ad libitum. Intake of ME ad libitum (3 weeks) increased cardiac protein of cytochrome oxidase and endothelial-type nitric oxide synthase (P < 0.05), indicating adaptation of the heart to higher activity. Transient HR responses evoked by an antidiabetic drug (levcromakalim) revealed a linear positive correlation with relative LOOH (r2 0.79), supporting the relationship between oxidative metabolic rate and lipoperoxidation. Evidence for exogenous lipids as LOOH source provided the vessel-specific rise in LOOH through replacing carbohydrate ME by lipid ME (Expt 2). Thus, dietary energy level and energetic source are important for circulatory LOOH with a role of vascular activity in production of oxidant.