ABSTRACT. Background. Peroxides have been reported to contaminate lipid emulsions and amino acid solutions used in total parenteral nutrition (TPN). This is particularly disturbing in newborn infants who are prone to several diseases related to immature defense mechanisms against oxidative challenges. It is not clear whether the antioxidants in multivitamins help protect parenteral nutrients against the hazards of oxidation.Objective. To evaluate the role of a multivitamin preparation (MVI) on the actual peroxide load received by patients on TPN.Methodology. The generation of peroxides in parenteral nutrition was tested first using test solutions. We compared the relative contribution of commercially available amino acid solutions, a lipid emulsion, and MVI on the level of peroxides in clinically relevant TPN solutions. Second, we measured the level of peroxides actually infused at the bedside. In both circumstances, the effects of time and light exposure were isolated. The level of peroxides was determined by a colorimetric technique and expressed as M equivalents tert-butyl hydroperoxide (M ‫؍‬ TBH).Results. Even when protected from light, the addition of MVI produced a 10-fold increase in peroxides (mean ؎ SEM, n ‫؍‬ 3, 19 ؎ 4 to 189 ؎ 8 M ‫؍‬ TBH at 4 h) in the fat-free TPN solution and a fourfold increase (64 ؎ 6 to 244 ؎ 8 M ‫؍‬ TBH at 4 h) in the lipid-containing TPN solution. A dose-response relationship was found between the concentration of MVI and peroxide levels. The effect of light was the strongest in the presence of multivitamins. The amino acid solutions had a relative inhibitory effect on the generation of peroxides by MVI, which varied (from 54 ؎ 1% to 72 ؎ 1%) all according to the amino acid blend. In parenterally fed premature infants, protecting the intravenous set from light decreased the load of infused peroxides (146 ؎ 15 vs 215 ؎ 24 M ‫؍‬ TBH).Conclusions. The lipid emulsion had a significant but minor additive effect compared with the multivitamin preparation, which was the major contributor to the generation of peroxides. Protection from photooxidation is not sufficient to prevent peroxidation of TPN solutions. Contrary to what one would expect, increasing the concentration of MVI will lead to a greater generation of peroxides, suggesting that the essential antioxidants in MVI do not have antiperoxide properties. Pediatrics 1997;99(3). URL: http://www.pediatrics.org/cgi/content/ full/99/3/e6; amino acids, antioxidants, detergents, lipids, newborn infants, oxidation, parenteral nutrition.ABBREVIATIONS. TPN, total parenteral nutrition; TBH, tert-butyl hydroperoxide; PN, fat-free and vitamin-free parenteral nutrition; MVI, multivitamin preparation.Isolated constituents of total parenteral nutrition (TPN) represent a potential source of oxidants. Because lipids infused with TPN solutions are contaminated by peroxides, 1,2 these emulsions are often believed to be the major source of oxidants in solutions of parenteral alimentation. However, other nutrients can promote peroxidation such as a...

In vitro, bilirubin is a strong antioxidant, but in vivo its capacity to act as a scavenger of toxic oxygen radicals remains poorly documented. The aim of this study was to evaluate if bilirubin had antioxidant properties in jaundiced infants. The antioxidant capacity of neonatal plasma was measured in Trolox equivalents (TEAC, mmol/l) and correlated in vitro with plasma bilirubin concentrations (r² = 0.99). Plasma TEAC was compared before and after exchange transfusions for neonatal hyperbilirubinemia (250–435 μmol/l). The antioxidant properties of the paired blood samples before and after exchange transfusions (TEAC: 1.67 ± 0.12 vs. 1.37 ± 0.09 mmol/l, n = 11) varied in proportion to the serum bilirubin levels. The changes in other antioxidants were not large enough to account for the magnitude of change in antioxidant capacity. Therefore, in vivo, the plasma antioxidant capacity of jaundiced newborn infants is related to the level of bilirubin.

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Hepatitis C virus (HCV) is a global health problem and a leading cause of liver disease. Here, we demonstrate that the replication of HCV replicon RNA in Huh-7 cells is inhibited by a peroxisome proliferator-activated receptor (PPAR) antagonist, 2-chloro-5-nitro-N-(pyridyl)benzamide (BA). Downregulation of PPARgamma with RNA interference approaches had no effect on HCV replication in Huh-7 cells, whereas PPARalpha downregulation inhibited HCV replication. Fluorescence and coherent anti-Stokes Raman scattering (CARS) microscopy demonstrate a clear buildup of lipids upon treatment with BA. These observations are consistent with the misregulation of lipid metabolism, phospholipid secretion, cholesterol catabolism, and triglyceride clearance events associated with the inhibition of PPARalpha. The inhibition of HCV replication by BA may result from disrupting lipidation of host proteins associated with the HCV replication complex or, more generally, by disrupting the membranous web where HCV replicates.

MIST for respiratory distress syndrome management in moderate and late preterm infants was associated with a significant reduction of MV exposure and pneumothorax occurrence.