Interaction between ascorbate and lightexposed riboflavin induces lung remodeling. The Journal of pharmacology and experimental therapeutics. 2004;311(2):634-9. Epub 2004/07/16

ABSTRACT Light-exposed parenteral multivitamins induce in lungs peroxidelike oxidant responses as well as the initiation of fibrosis. We hypothesized that peroxides generated in light-exposed total parenteral nutrition (TPN) affect lung remodeling. The objective was to assess the specific roles of peroxides, multivitamin preparation (MVP), and light exposure on lung remodeling during TPN. Threeday-old guinea pigs fitted with an indwelling catheter were assigned to the following intravenous regimens: TPN or MVP Ϯ photoprotection, H 2 O 2 Ϯ glutathione, MVP Ϯ metabisulfite, or ascorbic acid Ϯ riboflavin. Fed animals served as controls. After 4 days, lungs were sampled to determine alveolarization (intercepts), ␤-actin mRNA (protection assay), and apoptosis (terminal deoxynucleotidyl transferase dUTP nick-end labeling). Data were analyzed by analysis of variance. The infusion of light-exposed multivitamins induced a 20% lower (p Ͻ 0.01) alveolarization index than fed controls, and 3-fold higher (p Ͻ 0.01) apoptotic events. This was prevented by photoprotecting TPN. The effect of multivitamins on the alveolarization index was reproduced (p Ͻ 0.05) by infusion of light-exposed riboflavin in the presence of vitamin C. The alveolarization index correlated (r 2 ϭ 0.35; p Ͻ 0.05) with ␤-actin mRNA, suggesting alveolar disruption. Antiperoxides conferred no protection against decreased alveolarization. Lung remodeling induced by exposure of TPN to ambient light is not due to a direct effect of infused peroxides but rather to an interaction between vitamin C and peroxides generated by the exposure of riboflavin to light. It is speculated that this interaction may play a role in the development of chronic lung disease of premature infants who receive TPN and have immature antioxidant defenses

Light-Induced Byproducts of Vitamin C in Multivitamin Solutions

International audienceAbstract Background: When solutions of multivitamin preparations (MVPs) are exposed to light, H2O2 as well as organic peroxides are generated and the concentration of vitamin C decreases. The aim of this study was to determine, using mass spectrometry, whether the generation of oxidative byproducts of vitamin C, such as dehydroascorbate (DHA) and 2,3-diketogulonic acid (DKG), accounted for the reported decrease in ascorbic acid in MVPs exposed to light. Methods: Mass spectrometry was used to document the formation of byproducts of ascorbic acid in solutions containing a MVP, vitamin C + riboflavin, and vitamin C + H2O2 + Fe2+. The involvement of ascorbic acid and H2O2 in the formation of organic peroxides was tested by measuring peroxide concentrations in solutions containing H2O2 with or without ascorbic acid and with or without Fe2+ before and after addition of catalase. Results: The loss of ascorbic acid in photo-exposed MVPs was associated with the concomitant generation of byproducts different from DHA and DKG. Among them, one mass fingerprint was particularly observed with solutions of vitamin C + riboflavin exposed to ambient light as well as with the solution of vitamin C + H2O2 + Fe2+, suggesting a Fenton-like reaction. This fingerprint was associated with the formation of catalase-resistant peroxides. Conclusion: Exposure of MVPs to light leads to the rapid loss of ascorbic acid and generation of specific byproducts that differ from DHA and DKG. The conversion of vitamin C into byproducts could be of biological importance in accounting for the decrease in ascorbic acid concentrations and the generation of organic peroxides in light-exposed MVPs

Shielding parenteral multivitamins from light increases vitamin A and E concentration in lung of newborn guinea pigs

Background & aims: Exposure of parenteral multivitamin preparation (MVP) to light generates peroxides. Light-exposed MVP induces an oxidant stress in lung but not in liver. This discrepancy suggests differences in handling of infused antioxidant vitamins between the two organs. Hypothesis: antioxidant capacity of lung depends on the MVP concentration and light protection of infused solutions. Methods: Protocol 1: four groups of three-day old guinea pigs received the base solution (5% dextrose + 0.45% NaCl) enriched with 0%, 1%, 2% and 3% MVP. Protocol 2: three further groups received the base solution + 2% MVP either light-exposed or light-protected or light-protected + 300 μM H2O2. After 4 days, lung and liver were sampled for vitamin determinations. Data were analyzed by ANOVA. Results: In lung, vitamins A-C-E reached a plateau with 1% MVP. In liver, vitamin A and E increased according to their concentration in solutions. Light exposure and added-H2O2 were associated with lower vitamin E in lung and liver. Retinol was higher in lung and lower in liver of animals receiving light-protected compared to light-exposed solutions. Conclusions: Light protection of 1% MVP is a better way to improve the pulmonary oxidant-antioxidant balance than to increase MVP (>1%) in parenteral nutrition