Urinary N-Acetyl-β-D-glucosaminidase Isoenzymes as Biomarker of Renal Dysfunction Caused by Cadmium in a General Population

Jin, Taiyi; Nordberg, Gunnar F.; Wu, Xunwei; Ye, Tingting; Kong, Qinghu; Wang, Zaijuan; Zhuang, F.; Cai, S.

doi:10.1006/enrs.1999.3959

Cited by 76 publications

(47 citation statements)

References 13 publications

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“…An association between AAP and urinary cadmium was previously observed in studies of individuals with high occupational exposures (7,11), and NAG has been used as a marker of cadmium nephrotoxicity in several occupational and environmental studies (7,(10)(11)(12)33,34).…”

Section: Discussionmentioning

confidence: 80%

Effects of exposure to low levels of environmental cadmium on renal biomarkers.

Noonan

Sarasua

Campagna

et al. 2002

Environ Health Perspect

149

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We conducted a study among residents of a small community contaminated with heavy metals from a defunct zinc smelter and residents from a comparison community to determine whether biologic measures of cadmium exposure were associated with biomarkers of early kidney damage. Creatinine-adjusted urinary cadmium levels did not differ between the smelter and comparison communities; thus we combined individuals from both communities (n = 361) for further analyses. The overall mean urinary cadmium level was low, 0.26 microg/g creatinine, similar to reference values observed in the U.S. general population. For children ages 6-17 years, urinary concentration of N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), and albumin were positively associated with urinary cadmium, but these associations did not remain statistically significant after adjusting for urinary creatinine and other potential confounders. For adults ages 18 or older, urinary concentration of NAG, AAP, and albumin were positively associated with urinary cadmium. The associations with NAG and AAP but not with albumin remained statistically significant after adjusting for creatinine and other potential confounders. We found a positive dose-effect relationship between levels of creatinine-adjusted urinary cadmium and NAG and AAP activity, and statistically significant differences in mean activity for these two enzymes between the highest (> or =1.0 microg cadmium/g creatinine) and the lowest (< or =0.25 microg cadmium/g creatinine) exposure groups. The findings of this study indicate that biologic measures of cadmium exposure at levels below 2.0 microg/g creatinine may produce measurable changes in kidney biomarkers.

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Section: Discussionmentioning

confidence: 80%

Effects of exposure to low levels of environmental cadmium on renal biomarkers.

Noonan

Sarasua

Campagna

et al. 2002

Environ Health Perspect

149

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“…Cadmium exposure of general population in China and other Asian countries is generally higher than in Europe and the United States, because of the large number of cadmium-polluting industries and high intake of rice and vegetables grown locally in cadmium-contaminated soil [25,26]. Marked dose-dependent association between urinary cadmium levels and prevalence of renal dysfunction was observed in the population of cadmium polluted areas of southern China [27][28][29]. Prevention of environmental and occupational cadmium exposure is still a major public concern in China.…”

Section: Discussionmentioning

confidence: 93%

Cadmium Exposure is Associated with the Prevalence of Dyslipidemia

Zhou¹,

Lu²,

Pi³

et al. 2016

Cell Physiol Biochem

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Background: Cadmium is a widespread environmental and occupational pollutant that accumulates in human body with a biological half-life exceeding 10 years. Cadmium exposure has been demonstrated to increase rates of cardiovascular diseases. Whether occupational cadmium exposure is associated with the increase in the prevalence of dyslipidemia and hence contributes to the risk of cardiovascular diseases is still equivocal. To test the hypothesis that exposure to cadmium is related to the prevalence of dyslipidemia, we examined the associations between blood cadmium concentration and the prevalence of dyslipidemia in workers occupationally exposed to cadmium in China. Methods: A cross-sectional survey on demographic data, blood cadmium level and lipid profile in cadmium exposed workers from seven cadmium smelting factories in central and southwestern China was conducted. We measured blood cadmium concentration and lipid components of 1489 cadmium exposed workers. The prevalence of dyslipidemia was compared across blood cadmium quartiles. Associations between the blood cadmium concentrations and the prevalence of dyslipidemia were assessed using confounder adjusted linear and logistic regressions. Results: The blood cadmium concentration was 3.61±0.84µg/L ( mean ±SD). The prevalence of dyslipidemia in this occupational population was 66.3%. Mean blood cadmium concentration of workers with dyslipedemia was significantly higher than that of workers without dyslipidemia (p <0.01). The prevalence of dyslipidemia increased dose-dependently with elevations in blood cadmium concentrations (p for trend <0.001). Elevated levels of blood cadmium were associated with BMI, education attainment, income, smoking status and duration of exposure (all p <0.01). Furthermore, the profile of blood lipid was obviously changed in this occupational population. The prevalence of high TC, high TG, Low HDL-C and high LDL-C rose with increases in blood cadmium levels dose-dependently (p for trend <0.001). The odds ratios (95% confidence interval) for dyslipidemia across the increasing blood cadmium quartiles were 1.21(1.16-1.55), 1.56(1.11-1.87), 1.79(1.26-2.25) respectively (referencing to 1.00; p for trend <0.001), after multivariate adjustment for BMI, education attainment, income, lifestyle factors and duration of exposure, the association between blood cadmium concentrations and the prevalence of dyslipidemia remained unchanged (all p for trend <0.001). Conclusion: Elevated blood cadmium concentration is associated with prevalence of dyslipidemia. Cadmium exposure could alter lipid metabolism in humans. It is imperative to control cadmium exposure of occupational population in cadmium related industries and reduce adverse health effects.

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“…NAG-B is an intralysosomal membrane-bound enzyme, which is released into urine when disruption of lysosomal membranes occurs. NAG-T and especially NAG-B were reported as highly sensitive indicators of Cd tubular toxicity, and thus they were recommended for the biological monitoring of exposure to this heavy metal (Bernard et al 1995;Mueller et al 1998;Jin et al 1999;Price et al 1999). The Cd-induced increase in NAG-T and NAG-B urinary activities considerably preceded the occurrence of changes in other biochemical markers of kidney status.…”

Section: Discussionmentioning

confidence: 96%

“…The nephrotoxicity of Cd has been extensively studied and widely reported in occupationally (Kahan et al 1992;Bernard et al 1995;Ja¨rup et al 2000) and environmentally (Jin et al 1999;Price et al 1999;Ja¨rup et al 2000) exposed human subjects, as well as in various experimental models (Aughey et al 1984;Nordberg et al 1994;Mitsumori et al 1998;Ohta et al 2000). However, reports concerning the simultaneous assessment of the structure and function of this organ and Cd accumulation are rare.…”

Section: Introductionmentioning

confidence: 97%

“…The level of Cd above which early effects occur is unknown. Thus, special attention has been paid to evaluation of safe levels of Cd exposure in humans, and to search for sensitive biomarkers allowing detection of early changes at the stage when they are still reversible (Mueller et al 1998;Jin et al 1999;Price at al. 1999;Roels et al 1999).…”

Section: Introductionmentioning

confidence: 99%

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Changes in the structure and function of the kidney of rats chronically exposed to cadmium. I. Biochemical and histopathological studies

et al. 2003

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The aim of this study was to assess the effects of chronic exposure to cadmium (Cd) on the structure and function of kidneys, as well as to establish the body burden of Cd at which the changes occur. For this purpose we have created an experimental model using rats intoxicated with Cd administered in drinking water at the concentration of 5 or 50 mg Cd/l for 6, 12 and 24 weeks. The degree of kidney damage was evaluated biochemically and histopathologically. Sensitive biomarkers of Cd-induced proximal tubular injury such as urinary total N-acetyl-beta- d-glucosaminidase (NAG-T) and its isoenzyme B (NAG-B), and alkaline phosphatase (ALP) were used. Cd content in the kidney increased with the level and duration of exposure leading to dose- and time-dependent structural and functional renal failure. In rats exposed to 5 mg Cd/l, first symptoms of injury of the main tubules of long and short nephrons (structural damage to epithelial cells, increased urinary activities of NAG-T and NAG-B) were noted after 12 weeks of the experiment. The damage occurred at a low kidney Cd concentration amounting to 4.08+/-0.33 micro g/g wet weight (mean +/-SE) and a urinary concentration of 4.31+/-0.28 micro g/g creatinine. On exposure to 50 mg Cd/l, damage to the main tubules (blurred structure of tubular epithelium, atrophy of brush border, partial fragmentation of cells with release of nuclei into tubular lumen as well as increased urinary activities of NAG-T, NAG-B and ALP) was already evident after 6 weeks with the kidney Cd concentration of 24.09+/-1.72 micro g/g wet weight. In rats exposed to 50 mg Cd/l, a lack of regular contour of glomeruli was noted after 12 weeks, whereas after 24 weeks thickening of capillary vessels and widening of filtering space were evident. After 24 weeks of exposure to Cd, increased urea concentration in the serum with simultaneous decrease in its level in the urine, indicating decreased clearance of urea, and increased excretion of total protein were observed, but endogenous creatinine clearance remained unaffected. At the lower exposure, symptoms of structural, but not functional, damage to the glomeruli were also evident after 24 weeks of the experiment. Our results provide evidence that chronic exposure to Cd dose-dependently damages (structurally and functionally) the whole kidney. The injury affects the main resorptive part (proximal convoluted tubules and straight tubules) and the filtering part (glomeruli) of the nephron. But the target site for Cd action is the main tubule. We hypothesize that the threshold for Cd effects on the kidney is less than 4.08+/-0.33 micro g/g wet kidney weight and greater than 2.40+/-0.15 micro g/g (at this Cd concentration no symptoms of kidney damage were noted), and it may be close to the latter value. A very important finding of this study is that Cd acts on the whole kidney, especially on the main tubules, even at relatively low accumulation in this organ. It confirms the hypothesis that humans environmentally exposed to Cd, especially smokers, are at risk of t...

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Urinary N-Acetyl-β-D-glucosaminidase Isoenzymes as Biomarker of Renal Dysfunction Caused by Cadmium in a General Population

Cited by 76 publications

References 13 publications

Effects of exposure to low levels of environmental cadmium on renal biomarkers.

Effects of exposure to low levels of environmental cadmium on renal biomarkers.

Cadmium Exposure is Associated with the Prevalence of Dyslipidemia

Changes in the structure and function of the kidney of rats chronically exposed to cadmium. I. Biochemical and histopathological studies

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