Glyoxylate Oxidation and Enzymes of Oxalate Biosynthesis in Thiamine-Deficient Rats
Glyoxylic acid (GA) is the major precursor of endogenous oxalate and is mainly derived from glycine, glycolate and hydroxyproline. It can be either converted to C02 in liver and kidney mitochondria by TPP-dependent α-ketoglutarate:GA carboligase1 and via the glyoxylate oxidation cycle2, or it can be oxidized to oxalate by glycolic acid oxidase (GAO) and lactate dehydrogenase (LDH). Thiamine deficiency leads to excessive accumulation of GA in tissues and its increased excretion in urine3,4 and may result in a greater incidence of renal calculi5,6. There are, however, contradictory reports on the effect of thiamine deficiency on oxalate excretion7,8. The present study tries to elucidate the biochemical cause of the hyperoxaluria in thiamine deficiency.
KeywordsThiamine Deficiency Glyoxylic Acid Kidney Mitochondrion Urinary Citrate Excretion Pyridoxine Status
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