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This Article Full Text Full Text (PDF) All Versions of this Article: clinchem.2005.050427v1 51/8/1462    most recent Submit an electronic Letter to the Editor about this paper Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Knafo, L. Articles by Lavoie, J.-C. Search for Related Content PubMed PubMed Citation Articles by Knafo, L. Articles by Lavoie, J.-C. Related Collections Nutrition Lipids, Lipoproteins, and Cardiovascular Risk Factors Drug Monitoring and Toxicology

Association between Hydrogen Peroxide-Dependent Byproducts of Ascorbic Acid and Increased Hepatic Acetyl-CoA Carboxylase Activity

¹ Research Centre and Paediatric Department, CHU Sainte-Justine, University of Montreal, Montreal, Quebec, Canada.
² Division of Neonatology, Children’s and Women’s Health Centre of British Columbia, Vancouver, British Columbia, Canada.

^aAddress correspondence to this author at: Research Centre, CHU Sainte-Justine, 3175 Chemin Côte Ste-Catherine, Montreal, Qc, Canada H3T 1C5. Fax 514-345-4801; e-mail jean-claude.lavoie{at}umontreal.ca.

Background: Parenteral multivitamin preparation (MVP) induces fatty liver in neonatal guinea pig pups; this is prevented by photoprotection. Photo-excited riboflavin present in MVP generates H₂O₂ and molecules with masses of 136 and 208. We hypothesized that H₂O₂ initiates the peroxidation of ascorbic acid (AA), producing biologically active byproducts affecting hepatic lipid metabolism.

Methods: Mass spectrometry (MS) documented the participation of H₂O₂ and photo-excited riboflavin (Ribo) in the formation of AA byproducts. Sixteen 3-day-old guinea pig pups received an intravenous solution (50 g/L dextrose + 4.5 g/L NaCl + 1 kIU/L heparin) at 240 mL · kg^–1 · day^–1, enriched with control or test mixtures, for 4 days. The control mixture was photo-protected AA + Ribo (without byproducts or H₂O₂), and the test mixture was AA + Ribo treated to generate AA byproducts without H₂O₂. Hepatic acetyl-CoA carboxylase (ACC) activity was determined after 4 days. Fourth-day urine samples were analyzed by MS. Data were treated by ANOVA ( = 0.05).

Results: H₂O₂ did not influence the classic degradation of AA, as the generation of 2,3-diketogulonic acid was not affected. In contrast, the formation of molecules with masses of 136 and 208 was H₂O₂ and time dependent. ACC activity was higher (P <0.01) in animals receiving high concentration of these molecules; its hepatic activation correlated (P <0.01) with the urinary concentration of molecule-208.

Conclusions: H₂O₂ at concentrations found in the clinical setting of total parenteral nutrition induce the transformation of dehydroascorbic acid into compounds that have the potential to affect lipid metabolism. These molecules have peroxide and aldehyde functions.