N-Acetyl-P-D-glucosaminidases

Alkaline conditions are used so frequently in carbohydrate separations on CarboPac columns that it should be pointed out that acidic conditions are suitable for separation of acidic sugars. Figure 24 shows the separation of sialic acid containing oligosaccharides.256 Alkaline conditions were used for neutral milk oligosaccharides and mucin oligosaccharide alditols were characterized similarly.257 The carbohydrates released from yeast mannopro-tein with N-acetyl-P-D-glucosaminidase were also fractionated on CarboPac ... 

C. T. Yuen, P. R. N. Kind, R. G. Price, P. F. G. Praill, and A. C. Richardson, Colorimetric assay for N-acetyl-P-D-glucosaminidase (NAG) in pathological urine using the oo-nitrostyryl substrate the development of a kit and the comparison of the manual procedure with the automated fluorimetric method, Ann. Clin. Biochem., 21 (1984) 295-300. 

I. Pocsi, S. A. Taylor, A. C. Richardson, K. H. Aamlid, B. V. Smith, and R. G. Price, VRA-GlcNAc Novel substrate for N-acetyl-P-D-glucosaminidase applied to assay of this enzyme in human urine, Clin. Chem., 36 (1990) 1884-1888. 

In male Fischer 344 rats treated intraperitoneally with 0, 10, 20, 40, 60 or 80 mg/kg bw acrylonitrile, significant increases in urinary volume and glucose were observed 24 h after treatment with 20 mg/kg bw (Rouisse et al., 1986). Increased levels of urinary N-acetyl-P-D-glucosaminidase were detected after treatment with 60 mg/kg bw acrylonitrile. Symptoms of nephrotoxicity were also observ ed after a 4-h exposure to 200 ppm [434 mg/m3] acrylonitrile. Histopathological examination revealed lesions in the proximal tubular region of the kidney. 

Renal Effects. Occupational exposure to silver metal dust has been associated with increased excretion of a particular renal enzyme (N-acetyl-p-D glucosaminidase), and with decreased creatinine clearance (Rosenman et al. 1987). Both of these effects are diagnostic of marginally impaired renal function. However, the workers in this study were also exposed to cadmium, which was detected in the urine of 5 of the 27 workers studied. Cadmium is known to be nephrotoxic differentiation of the effects of the two metals in the kidney is not possible with the data presented. Therefore, no conclusion can be drawn regarding renal effects of silver based on this study. 

Occupational exposure to chromium(III) or chromium(O) does not appear to be associated with renal effects. No renal impairment based on urinary albumin, retinol binding protein, and renal tubular antigens was found in 236 workers employed in the ferrochromium production industry where ferrochromite is reduced with coke, bauxite, and quartzite. The mean airborne concentration of chromium in various sample locations was 0.075 mg chromium(III)/m3 chromium(VI) was below the detection limit of 0.001 mg chromium(VI)/m3 at all locations (Foa et al. 1988). Workers employed in an alloy steel plant with a mean exposure of 7 years to metallic chromium at 0.61 mg chromium(0)/m3 and to other metals had normal urinary levels of total protein and p2-microglobulin, enzyme activities of alanine-aminopeptidase, N-acetyl-P-D-glucosaminidase, gammaglutamyl-transpeptidase, and P-galactosi-dase (Triebig et al. 1987). In boilermakers exposed to chromium(O), no increase in urinary levels of... 

Urine Urinalysis with microscopic examinination of urine sediment Albumin Retinol binding protein N-acetyl-p-D-glucosaminidase Alanine aminopeptidase Osmolality Creatinine Glomerulus Proximal tubule Proximal tubule Proximal tubule Distal tubule Control for urine concentration... 

In LLC-PKj cells gentamicin induces membrane damage as shown by the loss of specific membrane enzymes (y-glutamyl transpeptidase, alkaline phosphatase and aminopeptidase), a decrease of the lysosomal enzyme N-acetyl-P-D-glucosaminidase, an inhibition of apical Na -dependent glucose transporter and the basolateral Na-K-ATPase pump as well as a decrease in dome formation [141, 142]. Furthermore gentamicin results in a dose dependent decrease in intracellular ATP and cAMP [142]. 

Treatment of rats with latamoxef (2000 mg/ g day) for 5 days induced an insignificant increase in the release of N-acetyl-p-D-glucosaminidase from lysosomes, when compared to control rats [81]. After intravenous treatment of rats with 1200 mg/kg/ d CPH for 3 days, homogenates of the renal cortex were separated into subcellular fractions and their protein composition was analyzed. The results of the SDS-gel electrophoresis of the renal cortical subtractions showed no relevant alterations of the polypeptide pattern in the lysosomal fraction [75]. 

Sugihira N, Saito H. Urinary excretion of N-acetyl-p-D-glucosaminidase and Pj-microglobulinin people living in a cadmium-polluted area. Jpn J Hyg 1986 41 665-671. 

Nogawa K, Yamada Y, Honda R,Tsuritani I, Ishizaki M, Sakamoto M. Urinary N-acetyl-p-D-glucosaminidase and Pj-microglobulin in itai-itai disease.Toxicol Lett 1983 16 317-322. 

N-acetyl-p-D-glucosaminidase (Figure 4). No significant correlation was evident for other renal parameters U-albumin, U-orosomucoid, U-p2-microglobulin, U-copper, S-creatinine, and S-p2-microglobulin. Studies on chlor-alkali workers in Scandinavia [122-124] have reported minimal and apparently reversible renal effects from mercury exposures in this occupational group as evaluated by urinary excrebon of NAG, albumin and titers of autoantibodies. These investigators noted that a small number of susceptible individuals may exist and that selenium status appears to have a major effect on urinary NAG excretion [124]. 

Bazzi C, Petr ini C, Rizza V, Arrigo G, Napodano P, PapareUa M, et al. Urinary N-acetyl-p-D-glucosaminidase excretion as a marker of tubular cell dysfunction and a predictor of outcome in primary glomerulonephritis. Nephrol Dial Transplant 2002 17 1890-6. 

Price RG. The role of NAG (N-acetyl-p-D-glucosaminidase) in the diagnosis of kidney disease including the monitoring of neplirotoxicity. Clin Nephrol 1992 38 S14-9. 

Endo G, Horiguchi S, Kiyota I. Urinary N-acetyl-p-D-glucosaminidase activity in lead-exposed workers. J AppI Toxicol 1990 10 235-238. 

USA [135]. In Germany, Jung et al. [136] reported increased prevalence of elevated urinary excretion of N-acetyl-P-D-glucosaminidase and retinol binding proteinuria both in occupationally and non- occupation-ally Cd exposed groups. In occupationally Cd exposed workers in Singapore [137] elevated levels of P2-... 

Nogawa K, Yamada Y Kido T, Honda R. Ishizaki M, Tsuritani I, Kobayashi E. Significance of elevated urinary N-acetyl-p-D-glucosaminidase activity in chronic cadmium poisoning. Sci Total Environ 1986 53 173-178. 

Roels et al. [38] points out that the analytical techniques identified in Table 1 are not easily available and are not well-suited for routine biomonitoring of occupational or environmental exposures. Instead, indirect biomarkers such as urinary enzymes are often used with success to evaluate mercury exposure and injury. Zalups [35] identifies numerous methods used to detect renal tubular injury induced by mercury. These methods monitor the urinary excretion of enzymes that leak from injured and necrotic proximal tubules, including lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and N-acetyl-P-D-glucosaminidase (NAG). Although advocated by Zalups (35) to detect renal tubular injury, Mason et al. (48) questions the practical utility of such biomarkers in occupational surveillance. According to Mason et al., small increases in NAG, leucine... 

Analysis of the tubular enzyme N-acetyl-P-D-glu-cosaminidase appears to be particularly effective in detecting early evidence of adverse renal effects from mercury [99, 100]. In an extensive cross sectional examination of chloralkali workers exposed to mercury at air concentrations around 25 fig/m, Langworth et al. [101] noted a significant correlation and dose-response relationship between urinary excretion of mercury and N-acetyl-P-D-glucosaminidase (Figure 4). No significant correlation was evident for other renal pa-... 

There are no reports of human nephrotoxicity caused by release of mercury from amalgam fillings. This is supported by experimental data from ten humans where standard measurements of renal function (glomerular filtrate rate, urinary albumin excretion, P2-microglobuUn, N-acetyl-P-D-glucosaminidase) were monitored before and 60 days after the removal of mercury amalgam fillings [102]. 

In a cross-sectional study by Boujemaa et al. [67], who evaluated early indicators of renal dysfunction in silicotic workers (n=116), recorded a delay after cessation of exposure up to 30 years (mean 23 years). The silicotic subjects excreted, on average, slightly higher amounts of albumin, retinol binding protein and N-acetyl-P-D-glucosaminidase [66, 67, 69]. 

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