8-iso-prostaglandin-a2 and Inflammation

Evidence suggests that higher plasma carotenoid concentrations are protective in relation to breast cancer recurrence. This simple randomized carrot juice intervention study was designed to test the hypothesis that daily intake of 8 ounces of fresh BetaSweet (anthocyanin-rich) or Balero orange carrot juice would increase plasma total carotenoid concentrations to levels previously shown to be associated with reduced breast cancer recurrence. It was hypothesized that regular carrot juice intake would be associated with reductions in oxidative stress (8-iso-PGF2α) and inflammation (thromboxane B2, prostaglandin E2 metabolites, and hsC-reactive protein). Sixty-nine overweight breast cancer survivors consumed fresh carrot juice made from study-provided carrots for 3 wk. Total plasma carotenoids increased by 1.65 and 1.38 umol/L for the BetaSweet and Balero carrot juice, respectively. Rise in total plasma carotenoids for the overall sample was inversely associated with 8-iso-PGFα (OR: 0.13; 95% CI: 0.20 to 0.75; no differences were shown by carrot variety. These results suggest daily intake of fresh carrot juice is a simple and effective approach to increasing plasma total carotenoids and in turn reducing oxidative stress, but not inflammatory markers, in women previously treated for breast cancer.

Topics: Adult; Aged; Anthocyanins; Beverages; Biomarkers; Breast Neoplasms; Carotenoids; Daucus carota; Female; Humans; Inflammation; Middle Aged; Neoplasm Recurrence, Local; Overweight; Oxidative Stress; Plant Tubers; Prostaglandins A; Survivors

Endotoxaemic challenge promptly causes lipid peroxidation. Porcine endotoxaemia can be used to replicate severe human septic shock. This model was used to evaluate non-enzymatic [8-Iso-prostaglandin F2alpha (8-Iso-PGF2alpha)] and enzymatic [15-keto-13,14-dihydro-prostaglandin F2alpha (15-K-DH-PGF2alpha)] lipid peroxidation, respectively, in relation to survival. The aim of this study was to correlate, if possible, pathophysiologic events during endotoxaemia to the levels of these arachidonic acid metabolites.. Nineteen pigs were anaesthetised, monitored (circulatory and respiratory variables in relation to lipid peroxidation) and given a continuous 6 h E. coli endotoxin (10 microg x kg(-1) x h(-1)) infusion. All animals were mechanically ventilated at constant tidal volumes and the inspired oxygen fraction was kept constant during the experimental period.. This endotoxin infusion caused expressed derangements in all pigs and death in 9 of them. The levels of 8-Iso-PGF2alpha, indicating oxidative injury, were different in time course, magnitude and fashion between survivors and non-survivors. The levels of 15-K-DH-PGF2alpha, indicating inflammatory response, showed a similar pattern. At 1 h the CO2 partial pressure in arterial blood was significantly higher in non-surviving pigs and correlated (r: 0.7; P<0.05) to the levels of 15-K-DH-PGF2alpha. Prostaglandin F2alpha is mainly metabolised in the lung. The lung weights were significantly (P<0.05) higher in non-surviving than in surviving animals. Both free radical and cyclooxygenase catalysed oxidative modification occurs during endotoxaemia.. Increased metabolism and inflammation, as evaluated by 15-K-DH-PGF2alpha, in the group of non-survivors may mediate the increase in arterial CO2. Thus, increased lipid peroxidation seems to be associated with endotoxaemic organ dysfunction and increased mortality.

Topics: Animals; Dinoprost; Endotoxemia; Female; Inflammation; Lipid Peroxidation; Male; Prostaglandins A; Swine; Time Factors