Effect of ascorbic acid deficiency on the in vivo synthesis of carnitine

• Published in: Biochimica et biophysica acta Vol. 672; no. 1; pp. 123 - 127
• Main Authors: Nelson, Peter J., Pruitt, Robert E., Henderson, LaRhee L., Jenness, Robert, Henderson, LaVell M.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 07.01.1981
• Subjects: Animals; ascorbic acid; Ascorbic Acid Deficiency - metabolism; Body Weight; Carnitine - biosynthesis; gamma-Aminobutyric Acid - analogs & derivatives; gamma-Aminobutyric Acid - metabolism; Guinea Pigs; Kidney - metabolism; Liver - metabolism; Lysine - analogs & derivatives; Lysine - metabolism; Male; Muscles - metabolism; Myocardium - metabolism; Organ Size
• ISSN: 0304-4165; 0006-3002; 1872-8006
• DOI: 10.1016/0304-4165(81)90286-5

The effects of ascorbate deficiency on carnitine biosynthesis was investigated in young male guinea pigs. Liver and kidney carnitine levels werenot affected by the defficiency, but scorbutic animals had 50% less carnitine in heart and skeletal muscle than control animals. Labeled carnitine precursors, 6-N- trimethyl- L-lysine and 4- N-trimethylaminobutt4yrate, both of which require ascorbate for their enzymatic hydroxylation, were injected into the vena cava of control, pair-fed and scorbutic animals. The distribution of isotope in compounds present in the liver and kidney after 1 h was determined. The uptake of trimethyllysine by the liver was <2% in 1 h, while the kidney took up approx. 20% of the 14C. Control and pair-fed animals converted trimethyllysine to kidney trimethylaminobutyrate 8–10 times as well as did scorbutic animals. Trimethylaminobutyrate hydroxylase, present in the liver but almost absent from the kidney, converted nearly all of substrate taken up by the liver to carnitine in both the scorbutic and control animals.