Abstract
A review of certain features of the carbohydrate metabolism of cornea is presented. The possible mechanisms oxidizing the reduced form of triphosphopyridine nucleotide (TPNH) generated in the hexose monophosphate shunt pathway are considered. One such mechanism is the oxidation of TPNH through the lactic dehydrogenase reaction. Evidence indicates that glucose oxidation through the shunt mechanism is inhibited by low levels of iodoacetate. Since oxidation through the citric acid cycle is not inhibited, the mechanism reoxidizing TPNH formed in the shunt mechanism appears to be different from that involved with the citric acid cycle. Moreover, the addition of pyruvate overcomes the iodoacetate inhibition of the shunt mechanism. These findings support the contention that oxidation of TPNH may proceed through the lactic dehydrogenase reaction. Certain requirements must be met before this mechanism can function under normal physiologic conditions: (1) diphosphopyridine nucleotide (DPN) must be in the oxidized form, or at least, DPNH must be of sufficiently low concentration so that it would not compete with TPNH for pyruvate; (2) a pH lower than 7.4 greatly enhances this mechanism; and (3) sufficient amounts of pyruvate must be present.