Abstract

The urinary excretion of N-acetyl-beta-D-glucosaminidase (U-NAG) and urinary Cadmium (U-Cd) concentration, a measure of the metal load in the body, were evaluated in 28 workers exposed to Cd, to determine the relation between the two parameters. In urine from 22 exposed workers with U-Cd<2 microg/g creatinine (Cr) there was no significant difference in U-NAG value (0.98+/-0.59 U/gCr) compared to non-exposed (0.73+/-0.48 U/gCr). In the six workers with 2 microg/gCr < or =U-Cd<10 microg/gCr the U-NAG (2.32+/-0.61 U/gCr) was statistically (P<0.05) higher than in other workers. In both the U-Cd intervals examined there were no altered values of beta2-microglobulin from urine of exposed workers compared to non-exposed (<0.30 mg/l). The U-NAG isoenzymes were separated by DEAE-cellulose chromatography from urine of non-exposed subjects and exposed workers. The U-NAG isoenzyme profile in urine of non-exposed subjects showed a high percentage (about 95%) of the A (acid) form, a much lower percentage (about 4.5%) of B (basic) form and a negligible percentage (about 0.5%) of I (intermediate) form. In the urine of 22 exposed workers with U-Cd<2 microg/gCr, the percentages of U-NAG isoenzymes were not different from non-exposed. In the urine of six workers with 2 microg/gCr< or =U-Cd<10 microg/gCr the percentage (8.34+/-0.91) of isoenzyme B (U-NAG-B), a marker of lesional enzymuria, was statistically increased (P<0.05) compared to non-exposed (4.42+/-0.56). These results suggest that adopting a biological limit for U-Cd equal to 10 microg/gCr might not be sufficiently protective. The increase in U-NAG-B content at 2 microg/gCr<U-Cd</=10 microg/gCr is probably due to a lesion of the proximal tubule caused by the metal which might follow an induction of the apoptotic process.