DISTURBANCE OF SIALIC-ACID METABOLISM BY CHRONIC CADMIUM EXPOSURE AND ITS RELATION TO PROTEINURIA

In workers exposed to Cd (8 years on the average), we have found a significant decrease of sialic acid in erythrocyte membranes (22.61 ± 1.84 vs 25.80 ± 3.01 μg/mg of protein in controls, p < 0.05) and an increase of sialic acid concentration in both urine (276.7 ± 132.3 vs 174.5 ± 70.9 μg/g of creatinine, p < 0.05) and plasma (761.8 ± 83.5 vs 640.4 ± 70.7 μg/ml, p < 0.01). In rats exposed to Cd (100 ppm in drinking water for 5.5 months), we have observed a reduction of the sialic acid level in erythrocyte membranes (31.4 ± 1.2 vs 33.4 ± 1.1 μg/mg of protein, p < 0.01) and glomeruli (12.5 ± 1.3 vs 13.9 ± 1.6 μg/mg of protein, p < 0.05). These effects in Cd treated rats were accompanied by a loss of the glomerular barrier selectivity as reflected by an increased urinary output of albumin and transferrin. After 10 months of Cd exposure, the albuminuria and transferrinuria were negatively correlated with sialic acid content of glomerular membranes (r = -0.47 and -0.51, p < 0.05), which suggests that the depletion of sialic acid is involved in the loss of glomerular barrier function induced by long term Cd exposure. In Cd-treated rats, sialidase activity was enhanced in kidney cortex and in serum but not in glomeruli. © 1991.