Light-Induced Byproducts of Vitamin C in Multivitamin Solutions

Lavoie, Jean-Claude; Chessex, Philippe; Rouleau, Thérèse; Migneault, Diane; Comte, Blandine

doi:10.1373/clinchem.2003.025338

Cited by 41 publications

(40 citation statements)

References 25 publications

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“…H 2 O 2 may induce programming of lipid and glucose metabolism. Indeed, other peroxides derived from lipids (47) or ascorbic acid (48) and differences in food intake may also be important confounding variables. Beyond a lack of mechanistic explanation, the study documents an effect of neonatal exposure to H 2 O 2 on metabolic programming.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Exposure to Oxidants Induces Later in Life a Metabolic Response Associated to a Phenotype of Energy Deficiency in an Animal Model of Total Parenteral Nutrition

et al. 2010

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Failure to protect total parenteral nutrition (TPN) from ambient light exacerbates the generation of peroxides, which affects blood glucose and plasma triacylglyceride (TG) in neonates. Based on the concept that the origin of adult diseases can be traced back to perinatal life, it was hypothesized that neonatal exposure to peroxides may affect energy availability later in life. Three-day-old guinea pigs, fitted with a jugular catheter, were fed regular chow (sham) Ϯ i. T he association between oxidative stress and characteristic features of the metabolic syndrome, such as diabetes, hypertension, and dyslipidemia, is well documented (1-6). Human (7) and animal studies (8,9) suggest that the origin of the metabolic syndrome can be traced back to perinatal life, a time when newborn infants are at greater risk of oxidative stress caused by weak antioxidant defenses (10 -12) or exposure to an oxidative environment or both (13-18). Several reports suggest that, in neonates, oxidative stress triggers the events that lead to programming of adult diseases (19 -22).Total parenteral nutrition (TPN) represents a source of oxidants in the form of peroxides that can be calibrated either by applying or not photoprotecting. The peroxides are derived from interactions between dissolved oxygen and electron donors such as lipid, amino acid, or ascorbic acid (23,24). The reaction is catalyzed by photoexcited riboflavin (24). Therefore, the main active agents participating in the generation of peroxides in TPN are ambient light [(ϩ)L] and multivitamin preparations (MVP) (23,24). Photoprotection [(Ϫ)L] of TPN reduces the levels of peroxides by close to 50% (23,25,26). Absence of photoprotection of TPN is associated in preterm newborn infants with higher urinary peroxide concentrations (16), higher blood pressure in girl babies (15), and greater blood glucose and plasma triacylglycerol concentrations (13). Hence, peroxides contaminating TPN solutions are not completely quenched by newborns infants and are thought to be an agent initiating metabolic perturbations. We questioned whether these peroxides are linked to metabolic consequences later in life.Based on the concept that neonatal oxidative stress may interfere with metabolic programming (27), we hypothesized that neonatal exposure to peroxides such as those generated in solutions of parenteral nutrition, induces a permanent modification in lipid and glucose metabolism especially lipogenesis and/or glycolysis. Perturbations in lipid and glucose metabolism, which are fuels for energy production, could have longterm consequences on growth and physical activity, thereby affecting global development. The aim of this study was to measure in adult guinea pigs metabolic responses and spontaneous physical activity after a brief neonatal exposure to i.v. oxidant molecules limited to the first wk of life. A second objective was to assess if these modifications were related to the infusion of peroxides. MATERIALS AND METHODSExperimental design. The metabolic response and the levels...

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Section: Discussionmentioning

confidence: 99%

Neonatal Exposure to Oxidants Induces Later in Life a Metabolic Response Associated to a Phenotype of Energy Deficiency in an Animal Model of Total Parenteral Nutrition

et al. 2010

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“…The predominant byproducts formed by oxidation or light degradation of AA (14,15,18 ) are DHA, DKG, molecule-136, and molecule-208; we therefore limited monitoring to AA, DKG, and molecules-136 and -208. Because the mass spectrometer was operated in negative mode, DHA was not detectable.…”

Section: In Vitro Studiesmentioning

confidence: 99%

“…Because the mass spectrometer was operated in negative mode, DHA was not detectable. We used DKG to monitor the classic oxidation of AA and used molecule-136 and its parent, molecule-208 (14 ), to monitor the peroxidation of AA. In the negative mode, AA, DKG, and molecules-136 and -208 have m/z of 175, 191, 135, and 207, respectively.…”

Section: In Vitro Studiesmentioning

confidence: 99%

“…As molecule-136 found in photoexposed MVP solutions derives from the byproduct molecule-208 and not from DKG (14 ), we suspected that it would be different from threonic acid. On the basis of previous reports (14,20 ), we hypothesized that the difference in reactions leading to the generation of molecule-136 and threonic acid resides in the presence of H 2 O 2 . In photo-exposed MVP, photo-excited riboflavin catalyzes transfer of electrons from a donor, such as AA, to oxygen, thereby generating hydrogen peroxide (H 2 O 2 ) (21 ).…”

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confidence: 96%

“…We suspected an ingredient of MVP that might be generated during light exposure. A mass spectroscopy (MS) study (14 ) led us to document the light-dependent formation of byproducts of ascorbic acid (AA), the most abundant of which had molecular masses of 136 and 208 (hereafter named molecule-136 and molecule-208).…”

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

et al. 2005

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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 (α = 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.

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Bohrer

2010

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Light-Induced Byproducts of Vitamin C in Multivitamin Solutions

Cited by 41 publications

References 25 publications

Neonatal Exposure to Oxidants Induces Later in Life a Metabolic Response Associated to a Phenotype of Energy Deficiency in an Animal Model of Total Parenteral Nutrition

Neonatal Exposure to Oxidants Induces Later in Life a Metabolic Response Associated to a Phenotype of Energy Deficiency in an Animal Model of Total Parenteral Nutrition

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

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