Mitochondrial oxidative metabolism during respiratory infection in riboflavin deficient mice

Studies in children and mice have shown that respiratory infection alters r iboflavin metabolism, resulting in increased urinary loss of this vitamin. This could be due to,mobilization of riboflavin from the liver to blood bec ause liver Flavin adenine dinucleotide (FAD) levels were lowered in the mic e during infection. To understand the functional implications of lowered he patic FAD levels during respiratory infection, flavoprotein functions such as oxidative phosphorylation and beta-oxidation of the liver mitochondria w ere examined during infection in mice. Weanling mice were fed either ribofl avin-restricted or control diet for 18 days and then injected with a sublet hal dose of Klebsiella pneumoniae. During infection, the state 3 respirator y rate with palmitoyl-L-carnitine and glutamate were significantly lowered (27-29%) in the riboflavin-restricted group, whereas in the control group 1 0% reduction was observed with palmitoyl-L-carnitine as substrate. A 22% re duction in the respiratory control ratio with palmitoyl-L-carnitine as subs trate was observed during infection in the riboflavin-restricted group. The beta-oxidation of palmitoyl-L-carnitine was significantly lower ecl (29%) in the riboflavin-restricted infected group. The results of the study sugge st that the effects of infection on vital physiologic functions were more p ronounced in the riboflavin-restricted mice than in the control mice. (C) E lsevier Science Inc. 1999. AII rights reserved.