Metabolic changes in the cornea of vitamin A-deficient rats.
We have investigated alterations of the metabolic state in vitamin A-deficient (A-) corneas using phosphorus-31 (31P) nuclear magnetic resonance (NMR) spectroscopy. Comparing to the control, A- corneas showed a prominent rise of phosphocreatine (PCr) as well as a total loss of glycerophosphorylcholine (GPC). Further, ATP levels were lower, and sugar phosphates (SP) and inorganic phosphate (Pi) were higher than those of the control. The accumulation of PCr and Pi, and decrease of ATP indicate that the activity of creatine kinase may be altered in vitamin A deficiency. These results suggest that vitamin A may have a role in creatine kinase activation and/or induction and that its deficiency causes a decline of energy metabolism in corneal epithelium. Moreover, disappearance of GPC implies an impaired cellular membrane metabolism. When retinyl acetate was supplied to A-rats for 5 weeks, the 31P profiles of vitamin A-repleted rat corneas recovered to normal.
Hayashi
K
K
Eye Research Institute of Retina Foundation, Boston MA 02114.
Cheng
H M
HM
Xiong
J
J
Xiong
H
H
Kenyon
K R
KR
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003315:Cornea / Q000378:metabolism*; D005997:Glycerylphosphorylcholine / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D010725:Phosphocreatine / Q000378:metabolism; D010758:Phosphorus; D051381:Rats; D011919:Rats, Inbred Strains; D013403:Sugar Phosphates / Q000378:metabolism; D014802:Vitamin A Deficiency / Q000378:metabolism*
D013403:Sugar Phosphates; D010725:Phosphocreatine; D010758:Phosphorus; D005997:Glycerylphosphorylcholine; D000255:Adenosine Triphosphate