METABOLIC BASIS OF OXALOSIS IN RATS MIMICKING TYPE-1 PRIMARY HYPEROXALURIA

In rats mimicking type 1 primary hyperoxaluric conditions, as a conseq uence of oral ingestion of glyoxylate, heightened activity of liver la ctate dehydrogenase led to excess formation of glycolate and oxalate. A similar rise in activity of liver glycolic acid oxidase resulted in the increased oxidation of glycolate --> glyoxylate --> oxalate with t he concomitant production of H2O2. Parallel with these changes, the ac tivities of glutathione peroxidase and catalase declined in liver and kidneys, accounting for the enhanced lipid peroxidation potential seen in these tissues. Oral administration of antioxidants such as glutath ione or methionine prevented the glyoxylate-induced hyperoxaluria and also the manifestation of renal necrosis.