Jean-Claude Lavoie , Ph.D.
    Jean-Claude Lavoie
    Research Axis
    Metabolic and Cardiovascular Health Axis
    Research Theme
    Energy metabolism, stress and mitochondrial dysfunction
    CHUSJ - Centre de Recherche

    514 345-4931 #3940

    514 345-4801


    • Associate Professor, Department of Pediatrics, University of Montreal, 2008.


    • PhD in Biomedical Science, University of Montreal, 1998.
    • MSc in Biomedical Science, University of Montreal, 1992.
    • DESS in Toxicology, University of Montreal, 1989.

    Research Interests

    Imbalance between the antioxidant defense capacity and the oxidant load received by infants is thought to be an important factor in several neonatal complications of prematurity of which the incidence and morbidity of some are gender-dependent. The validation of this hypothesis has been the center of my studies for the last 10 years. The deficit in antioxidant ability was demonstrated by the low concentrations of glutathione (a key antioxidant molecule) found in cells from premature newborns, especially males.

    This low glutathione level is not linked to synthesis or regeneration but rather to an immature transcellular transport of cysteine (substrate for glutathione synthesis). Parenteral nutrition contains a high oxidant load. Parenteral multivitamins exposed to ambient light are the main source of peroxides in parenteral nutrition. They are generated by a reaction between dissolved oxygen and ascorbic acid, then in turn catalyzed by photo-activated riboflavin. The infusion of light-exposed multivitamin preparations in animals induces the onset of pulmonary fibrosis (caused by peroxides), accompanied by low alveolarization (caused as a result of vitamin C degradation), as well as hepatic steatosis and hypertriglyceridemia. Our studies have shown that photoprotected parenteral nutrition prevents elevated levels of urinary peroxides and hypertriglyceridemia in children. Through mass spectrometry, we have also found a new vitamin C degradation pathway which leads to the formation of ascorbylperoxide. In animals, urinary concentrations of this new molecule are correlated with hepatic acetyl CoA carboxylase, a key enzyme in the synthesis of fatty acids.


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