Ascorbylperoxide Contaminating Parenteral Nutrition Perturbs the Lipid Metabolism in Newborn Guinea Pig

The light exposure of parenteral nutritive solutions generates peroxides such as H 2 O 2 and ascorbylperoxide [2,3-diketo-4-hydoxyperoxyl-5,6-dihydroxyhexanoic acid]. This absence of photoprotection is associated with higher plasma triacylglycerol (TG) concentration in premature infants and oxidative stress and H 2 O 2 -independent hepatic steatosis in animals. We hypothesized that ascorbylperoxide is the active agent leading to high TG. The aim was to investigate the role of ascorbylperoxide in glucose and lipid metabolism in an animal model of neonatal parenteral nutrition. Three-day-old guinea pigs received through a catheter in the jugular solutions containing dextrose plus 0, 90, 225, or 450 μM ascorbylperoxide. After 4 days, blood and liver were sampled and treated for determinations of TG, cholesterol, markers of oxidative stress (redox potential of glutathione and F 2α -isoprostane), and activities and protein levels of acetyl-CoA carboxylase (ACC), glucokinase, and phosphofructokinase (PFK). Ascorbylperoxide concentration was measured in urine on the last day. Data were compared by analysis of variance ( p r 2 = 0.69) and hepatic PFK activity ( r 2 = 0.26) were positive, whereas they were negative with ACC activity ( r 2 = 0.50). In conclusion, ascorbylperoxide contaminating parenteral nutrition stimulates glycolysis, allowing higher availability of substrates for lipid synthesis. The logarithmic relation between urinary ascorbylperoxide and plasma TG suggests a very low efficient concentration.