. 13 , No . 2 ( 2004 ) , 121-125 Urinary Activities of N-acetyl-β-D-glucosaminidase and Its Isoenzyme B in Cadmium-Exposed Rats

This paper aims to assess the relationship between the urinary activity of N-acetyl-β-D-glucosaminidase (NAG) and its isoenzyme B (NAG-B) and cadmium (Cd) concentration in the urine as well as to evaluate which of these lysosomal enzymes may be a more useful biomarker for the monitoring of Cd-induced tubular damage. For this purpose we have used an experimental model in rats chronically exposed to Cd in which we noted damage to the proximal tubules, including lysosomes. In rats intoxicated with 5 mg Cd/dm3, the urinary activities of NAG and NAG-B increased after 12 weeks of treatment, while at 50 mg Cd/dm3 activities increased already after the 1st week. The urinary Cd excretion in Cd-exposed rats, but not in the non-exposed ones, positively correlated with the activities of NAG and NAG-B. A positive correlation which was observed between NAG and NAG-B activities was stronger in Cd-exposed animals than in those not exposed. The results of the present and our previous histopathological and histoenzymatic studies, confirm the usefulness of total NAG and NAG-B as sensitive markers of proximal tubular injury for the monitoring of chronic exposure to Cd. Taking into account the strong correlation between the total NAG and its isoenzyme B, similar correlation coefficients between their activities and Cd concentration in urine and simplicity of total NAG determination compared to that of NAG-B, one can conclude that the determination of total NAG is suitable for the monitoring of exposure to Cd. As the urinary activity of total NAG is a sum of activities of several isoenzymes, which may be influenced by various factors, and the intralysosomal localization of NAG-B, we hypothesize that NAG-B should be recommended as a sensitive and useful marker for routine monitoring of chronic exposure to Cd.

[1]  K. Zwierz,et al.  Isoenzymes of N-acetyl-β-hexosaminidase in human pleomorphic adenoma and healthy salivary glands: a preliminary study , 2008, Clinical chemistry and laboratory medicine.

[2]  C. Tohyama,et al.  Increased urinary cadmium excretion and its relationship to urinary N-acetyl-β-d-glucosaminidase activity in smokers , 2005, Archives of Toxicology.

[3]  O. Sugita.  [Urinary N-acetyl-beta-D -glucosaminidase]. , 2004, Nihon rinsho. Japanese journal of clinical medicine.

[4]  K. Zwierz,et al.  Changes in the structure and function of the kidney of rats chronically exposed to cadmium. I. Biochemical and histopathological studies , 2003, Archives of Toxicology.

[5]  M. Brzóska,et al.  Cadmium turnover and changes of zinc and copper body status of rats continuously exposed to cadmium and ethanol. , 2002, Alcohol and alcoholism.

[6]  P. Mueller,et al.  Effects of exposure to low levels of environmental cadmium on renal biomarkers. , 2002, Environmental health perspectives.

[7]  P. Allain,et al.  Blood cadmium concentration in the population of the Rabat area, Morocco. , 2000, Clinica chimica acta; international journal of clinical chemistry.

[8]  L Järup,et al.  Low level exposure to cadmium and early kidney damage: the OSCAR study , 2000, Occupational and environmental medicine.

[9]  H. Nakagawa,et al.  Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. , 2000, Environmental research.

[10]  L. Feligioni,et al.  Activity and isoenzyme profile of N-acetyl-beta-D-glucosaminidase in urine from workers exposed to cadmium. , 2000, Clinica chimica acta; international journal of clinical chemistry.

[11]  D. Lison,et al.  Usefulness of biomarkers of exposure to inorganic mercury, lead, or cadmium in controlling occupational and environmental risks of nephrotoxicity. , 1999, Renal failure.

[12]  P. Morucci,et al.  Blood cadmium concentrations in the general population of Umbria, central Italy. , 1999, The Science of the total environment.

[13]  R. G. Price,et al.  Early markers of nephrotoxicity: detection of children at risk from environmental pollution. , 1999, Renal failure.

[14]  M. Krzyzanowski,et al.  Cadmium content in human kidney and hair in the Gdańsk region. , 1998, The Science of the total environment.

[15]  K. Mitsumori,et al.  Relationship between the development of hepato-renal toxicity and cadmium accumulation in rats given minimum to large amounts of cadmium chloride in the long-term: preliminary study , 1998, Archives of Toxicology.

[16]  J. Richmond,et al.  Measurement of vitamin D3 metabolites in smelter workers exposed to lead and cadmium. , 1998, Occupational and environmental medicine.

[17]  P. Mueller,et al.  New approaches for detecting thresholds of human nephrotoxicity using cadmium as an example. , 1998, Environmental health perspectives.

[18]  H. Roels,et al.  Association between NAG-B and cadmium in urine with no evidence of a threshold. , 1995, Occupational and environmental medicine.

[19]  M. Nordberg,et al.  Subcellular targets of cadmium nephrotoxicity: cadmium binding to renal membrane proteins in animals with or without protective metallothionein synthesis. , 1994, Environmental health perspectives.

[20]  H. Ralston.  The use of animals in biomedical research. , 1988, Archives of internal medicine.

[21]  A. Giles,et al.  Guidelines for the use of Animals in Biomedical Research , 1987, Thrombosis and Haemostasis.

[22]  K. Zwierz,et al.  The degradation of glycoconjugates in the human gastric mucous membrane. , 1981, Acta medica Academiae Scientiarum Hungaricae.