Studies in children and mice have shown that respiratory
infection alters
riboflavin metabolism, resulting in increased urinary loss of this
vitamin. This could be due to mobilization of
riboflavin from the liver to blood because liver
Flavin adenine dinucleotide (
FAD) levels were lowered in the mice during
infection. To understand the functional implications of lowered hepatic
FAD levels during respiratory
infection,
flavoprotein functions such as oxidative phosphorylation and beta-oxidation of the liver mitochondria were examined during
infection in mice. Weanling mice were fed either
riboflavin-restricted or control diet for 18 days and then injected with a sublethal dose of Klebsiella pneumoniae. During
infection, the state 3 respiratory rate with palmitoyl-
L-carnitine and
glutamate were significantly lowered (27-29%) in the
riboflavin-restricted group, whereas in the control group 10% reduction was observed with palmitoyl-
L-carnitine as substrate. A 22% reduction in the respiratory control ratio with palmitoyl-
L-carnitine as substrate was observed during
infection in the
riboflavin-restricted group. The beta-oxidation of palmitoyl-
L-carnitine was significantly lowered (29%) in the
riboflavin-restricted infected group. The results of the study suggest that the effects of
infection on vital physiologic functions were more pronounced in the
riboflavin-restricted mice than in the control mice.