Hypovitaminose c is associated with alterations in plasma carnitine metabolism

Vitamin C is an essential cofactor in the biosynthesis of carnitine. Carnitine is necessary for the transport of long chain fatty acids into the mitochondria for energy utilization. Currently, there are no functional markers for vitamin C nutriture. We examined whether plasma carnitine was a marker of vitamin C status. Blood from healthy, non-smoking college students (n=135; m = 62, f=73) was analyzed for plasma vitamin C and plasma free carnitine. 'IVo percent of the sample population had plasma vitamin C levels indicative of scurvy; 18%, 34%, and 46% had subnormal, adequate, and ample plasma vitamin C levels respectively. Plasma free carnitine levels were elevated in the subnormal and adequate vitamin C groups in comparison to reference values. The plasma free carnitine in the ample vitamin C group was significantly less than the other groups (p< .05) and compared more closely to reference values. Plasma vitamin C status was inversely related to plasma carnitine levels (r = -0.30. p<.001). Others have demonstrated that although plasma and urinary carnitine is elevated in vitamin C deficiency, muscle carnitine is significantly reduced by 50-60%. Thus, our results imply that carnitine transport into the muscle tissue is impaired. Carnitine transport occurs in an exchange process with -y-hutyrohetaine, which is synthesized in muscle tissue. In the vitamin C depleted state, tissue γ-hutyrohelaine hydroxylase activity is reduced and tissue levels of the immediate precursor tu carnitine, -y-butyrobetaine rise. We conclude that vitamin C deficiency may he associated with impaired carnitine transport into muscle tissue in addition to impaired carnitine biosynthesis and,that the plasma free carnitine may prove to he a valuable marker of vitamin C status.