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Taiyi Jin

Publications and source records attributed to Taiyi Jin.

At least 19 recordsLinked to original sources
PubMed2006

p53-Dependent but ATM-independent inhibition of DNA synthesis and G2 arrest in cadmium-treated human fibroblasts.

This study focused on the activation of cell cycle checkpoint responses in diploid human fibroblasts that were treated with cadmium chloride and the potential roles of ATM and p53 signaling pathways in cadmium-induced responses. The alkaline comet assay indicated that cadmium caused a dose-dependent increase in DNA damage. Cells that were rendered p53-defective by expression of a dominant-negative p53 allele or knockdown of p53 mRNA were more resistant to cadmium-induced inactivation of colony formation than normal and ataxia telangiectasia (AT) cells. Synchronized fibroblasts in S were more sensitive to cadmium toxicity than cells in G1, suggesting that cadmium may target some element of DNA replication. Cadmium produced a dose- and time-dependent inhibition of DNA synthesis. An immediate inhibition was associated with severe delay in progression through S phase and a delayed inhibition seen 24 h after treatment was associated with accumulation of cells in G2. AT and normal cells displayed similar patterns of inhibition of DNA synthesis and G2 delay after treatment with cadmium, while p53-defective cells displayed significantly less of the delayed inhibition of DNA synthesis and accumulation in G2 post-treatment. Total p53 protein and ser15-phosphorylated p53 were induced by cadmium in normal and AT cells. The p53 transactivation target Gadd45alpha was induced in both p53-effective and p53-defective cells after 4 h cadmium treatment, and this was associated with an acute inhibition of mitosis. Cadmium produced a very unusual pattern of toxicity in human fibroblasts, inhibiting DNA replication and inducing p53-dependent growth arrest but without induction of p21(Cip1/Waf1) or activation of Chk1.

Ataxia Telangiectasia↗
PubMed2006

Critical exposure level of cadmium for elevated urinary metallothionein--an occupational population study in China.

Cadmium is a well-known nephrotoxic agent with extremely long biological half-time of 15-30 years in humans. To prevent nephrotoxicity induced by cadmium, it is necessary to identify specific and sensitive biomarkers of cadmium exposure and renal damage, and to define critical exposure levels related to minimal nephrotoxicity in humans. In this study, urinary cadmium (UCd) and blood cadmium (BCd) were used as cadmium exposure indicators, urinary beta(2)-microglobulin (UB2M), N-acetyl-beta-D-glucosaminidase (UNAG) and albumin (UALB) were applied as the effect biomarkers of tubular and glomerular dysfunction. The relationship between urinary metallothionein (UMT) and cadmium exposure biomarkers as well as effect biomarkers was examined. Significant correlations were found between the UMT and BCd, and UCd. At the same time, UB2M, UALB and UNAG showed positive correlation with UMT as well. According to this result, cadmium-exposed individuals with renal dysfunction excreted more metallothionein than those without. Dose-response relationships between UCd and urinary indicators of renal dysfunction were studied. The critical concentration of UCd was quantitatively estimated by the benchmark dose (BMD) method. The lower confidence limit of the BMD-10 (BMDL) of UCd (3.1 microg/g Cr) related to increased excretion of urinary metallothionein was slightly higher than that for UNAG (2.7 microg/g Cr), but lower than those of UB2M (3.4 microg/g Cr) and UALB (4.2 microg/g Cr). The results demonstrate that UMT may be used as a sensitive biomarker of renal tubular dysfunction in cadmium-exposed populations.

Cadmium↗
PubMed2006

Lung cancer development in primary smelter workers: a nested case-referent study.

OBJECTIVE: The objective of this study was to study the impact of work-related exposure to mainly arsenic and lead versus smoking in primary smelter workers developing lung cancer. METHODS: In a cohort of 3979 primary smelter workers, 46 subjects had contracted respiratory malignancies. They were compared with 141 age-matched male referents by conditional logistic regression analysis. RESULTS: Cases showed a significantly higher smoking rate as compared with referents: odds ratio (OR) = 4.0; 95% confidence interval (CI) = 1.6-10.1; P = 0.003. When restricted to smokers (33 cases, 63 referents), the cumulative air arsenic exposure index, but not the lead exposure indices, was significantly higher among the cases: OR = 1.07; 95% CI = 1.02-1.11; P = 0.005. CONCLUSIONS: Cumulative arsenic exposure and smoking were identified as risk factors for the development of lung cancer; lead exposure, however, was not.

Arsenic Poisoning↗
PubMed2006

Plasma metallothionein antibody, urinary cadmium, and renal dysfunction in a Chinese type 2 diabetic population.

OBJECTIVE: It has been reported that diabetes may increase the risk of cadmium-induced kidney damage. The presence of metallothionein antibody (MT-Ab) increased the susceptibility for tubular damage among cadmium workers. This study focused on the relationships between levels of MT-Ab, urinary cadmium, and kidney function in a Chinese type 2 diabetic population. RESEARCH DESIGN AND METHODS: A cross-sectional study was performed on 229 type 2 diabetic patients (92 men and 137 women) who were recruited from two community centers in one district of Shanghai City in China. Information was obtained from interviews, health records, and blood and urine samples. RESULTS: Levels of the tubular biomarker beta2-microglobulin increased significantly when the levels of MT-Ab and urinary cadmium were elevated in male and female subjects; in contrast, the levels of urinary albumin, a glomerular biomarker, did not display such a pattern. After adjusting for potential confounding covariates, logistic regression showed that the odds ratios (ORs) of tubular dysfunction increased upon 1) increasing the MT-Ab concentration from a low to high level (OR 5.56 [95% CI 2.25-13.73]) and 2) increasing the level of urinary cadmium from <1 to >or=1 microg/g creatinine (3.34 [1.17-9.53]); the OR of patients currently smoking was 3.51 (1.14-10.80) relative to that of those who had never smoked. CONCLUSIONS: This study proves that the presence of MT-Ab can potentiate tubular dysfunction among diabetic subjects and that patients with high MT-Ab levels are more prone to development of tubular damage.

Aged↗
PubMed2005

Plasma metallothionein antibody and cadmium-induced renal dysfunction in an occupational population in China.

It has been reported that anti-metallothionein (a metallothionein antibody) is present in the circulation of healthy subjects and in patients suffering from atopic dermatitis. The aim of this study was to investigate whether cadmium-induced renal dysfunction is related to the presence of the plasma metallothionein antibody (MT-Ab) in workers exposed to cadmium (Cd) occupationally. Plasma metallothionein antibody was determined by enzyme linked immunosorbent assay (ELISA) techniques, and both exposure assessment and risk assessment were conducted in cadmium-exposed workers in China. We demonstrate that there is a significantly increased prevalence of renal dysfunction with respect to the level of urinary cadmium in a dose-dependent manner. We found no significant correlations between the levels of MT-Ab and the external or internal exposure doses of cadmium (p > 0.05), but the levels of MT-Ab did correlate positively with two biomarkers of renal dysfunction-urinary beta2-microglobulin (UB2M; r = 0.218, p < 0.05) and N-acetyl-beta-D-glucosaminidase (UNAG; r = 0.302, p < 0.001)-in the cadmium-exposed workers. Workers who have high levels of MT-Ab display cadmium-induced tubular nephrotoxicity more frequently than those possessing low levels of MT-Ab; odds ratio (OR) 4.2; 95% confidence intervals 1.2-14.5 (p < 0.05). This study suggests that subjects that have higher MT-Ab levels more readily develop cadmium-induced renal dysfunction. Thus, the levels of plasma MT-Ab can be used as a biomarker of susceptibility to renal dysfunction in occupational cadmium exposure.

Adult↗
PubMed2005

Metallothionein gene expression in peripheral lymphocytes and renal dysfunction in a population environmentally exposed to cadmium.

In order to study the validity of metallothionein (MT) gene expression in peripheral blood lymphocytes (PBLs) as a biomarker of cadmium exposure and susceptibility to renal dysfunction, MT mRNA levels were measured using reverse transcription polymerase chain reaction (RT-PCR) in PBLs from residents living in a cadmium-contaminated area. MT mRNA levels were found to increase with the increase of blood cadmium (BCd) and urinary cadmium (UCd) levels. Basal MT mRNA levels were significantly correlated with the logarithm of BCd levels and the logarithm of UCd levels confirming that MT expression in PBLs is a biomarker of cadmium exposure and internal dose. An inverse relationship was observed between in vitro induced MT-mRNA level in PBLs and urinary N-acetyl-beta-d-glucosaminidase (UNAG) suggesting that MT gene expression in PBLs may be used as a biomarker of susceptibility to renal toxicity of cadmium.

Adult↗
PubMed2005

Lycopene inhibits the growth of human androgen-independent prostate cancer cells in vitro and in BALB/c nude mice.

Lycopene is a promising chemopreventive agent for human prostate cancer. To test the hypothesis that the effect of lycopene on prostate cancer is stage specific in the process of carcinogenesis, inhibitory effects of natural lycopene on the proliferation of 3 different human prostate carcinoma cell lines were examined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Lycopene more potently inhibited the growth of the androgen-independent DU145 and PC-3 cells than androgen-dependent LNCaP cells. The 50% inhibitory concentration of lycopene for these cell lines was 26.6 micromol/L for DU145, 40.3 micromol/L for PC-3, and 168.5 micromol/L for LNCaP. We also studied the inhibitory effect of lycopene on the growth rate of DU145 tumor xenografts in BALB/c male nude mice. The tumor growth rate was inhibited by 55.6 and 75.8% in mice treated with 100 and 300 mg/kg lycopene, respectively, compared with controls. In addition, no tumors formed in 1 mo in mice treated with DU145 cells that had been pretreated with 20 micromol/L lycopene; however, they did form when DU145 cells were not pretreated. Flow cytometry revealed that lycopene caused DU145 cells to accumulate in the G(0)/G(1) phase and to undergo apoptosis in a dose-dependent manner. The rate of apoptosis was up to 42.4% lower in DU145 cells treated with 32 micromol/L lycopene compared with the untreated control cells. These results suggest that lycopene may specifically inhibit the growth of androgen-independent prostate cancers.

Animals↗
PubMed2005

Genetic polymorphisms in XRCC1, APE1, ADPRT, XRCC2, and XRCC3 and risk of chronic benzene poisoning in a Chinese occupational population.

DNA damage induced by benzene is an important mechanism of its genotoxicity that leads to chronic benzene poisoning (CBP). Therefore, genetic variation in DNA repair genes may contribute to susceptibility to CBP in the exposed population. Because benzene-induced DNA damage includes single- and double-strand breaks, we hypothesized that single-nucleotide polymorphisms in X-ray repair cross-complementing group 1 (XRCC1), apurinic/apyrimidinic endonuclease (APE1), ADP ribosyltransferase (ADPRT), X-ray repair cross-complementing group 2 (XRCC2), and X-ray repair cross-complementing group 3 (XRCC3) are associated with risk of CBP. We genotyped single-nucleotide polymorphisms at codons 194, 280, and 399 of XRCC1, codon 148 of APE1, codon 762 of ADPRT, codon 188 of XRCC2, and codon 241 of XRCC3 in 152 CBP patients and 152 healthy workers frequency matched on age and sex among those who were occupationally exposed to benzene. The genotypes were determined by PCR-RFLP technique with genomic DNA. We found that no individuals had the XRCC2 codon 188 variant alleles or Met/Met genotype of XRCC3 codon 241 in this study population. However, individuals carrying the XRCC1 194Trp allele (i.e., Arg/Trp+Trp/Trp genotypes) had a decreased risk of CBP [adjusted odds ratio (OR(adj)), 0.60; 95% confidence interval (95% CI), 0.37-0.98; P = 0.041] compared with subjects with the Arg/Arg genotype whereas individuals carrying the XRCC1 280His allele (i.e., Arg/His+His/His genotypes) had an increased risk of CBP compared with those with the Arg/Arg genotype (OR(adj), 1.91; 95% CI, 1.17-3.10; P = 0.009). The analysis of haplotypes of polymorphisms in XRCC1 showed that there was a 2.96-fold (OR, 2.96; 95% CI, 1.60-5.49; chi(2) = 12.39, P = 0.001) increased risk of CBP for subjects with alleles of XRCC1 194Arg, XRCC1 280His, and XRCC1 399Arg compared with those carrying alleles of XRCC1 194Arg, XRCC1 280Arg, and XRCC1 399Arg. Therefore, our results suggest that polymorphisms at codons 194 and 280 of XRCC1 may contribute to CBP in a Chinese occupational population.

Adult↗
PubMed2004

Impact of cadmium exposure on male sex hormones: a population-based study in China.

The objective of this study was to investigate the possible effects of environmental cadmium (Cd) exposure on the levels of serum sex hormones in a Chinese population group. A total of 263 male volunteers were included. Blood samples were collected for the determination of serum testosterone (T), measured by radioimmunoassay, and follicle stimulating hormone (FSH) and luteinizing hormone (LH), both measured by enzyme immunoassays. Urinary and blood Cd were analyzed by atomic absorption spectroscopy (AAS). We found a dose-response relationship between urinary Cd excretion and the prevalence of abnormally high serum T levels, but, through multiple regression analysis, we could not trace exposure to Cd as a significant determinant of serum T levels. Exposure to Cd also failed to influence the levels of FSH and LH in serum. In contrast, we found that age, body mass index (BMI), and smoking habits are significant determinants of FSH and LH and of T and LH, respectively. We conclude that oral Cd exposure is not a critical determinant of hormone homeostasis in males, but lifestyle and some biological factors, such as age and BMI, are important. The relationship found between urinary Cd and high T levels may be of importance for male reproductive morbidity and should be investigated further.

Administration, Oral↗
PubMed2004

Osteoporosis and renal dysfunction in a general population exposed to cadmium in China.

Osteoporosis is a common metabolic disease characterized by low bone mass and microarchitectural deterioration of bone tissue. Many factors are involved in the occurrence of osteoporosis. Cadmium can cause both osteomalacia and osteoporosis and these effects have long been investigated through various epidemiological or experimental studies. The present study examines a possible relationship between cadmium nephropathy and its effects on the skeleton in populations living in a polluted area in southeast China. Monophoton absorptiometry was used to measure bone mineral density in the population and the Z score (the number of SD from the difference between the measured bone density of the individual and the group mean value for sex- and age-matched controls) was introduced to define osteoporosis (Z score < -2). Osteoporosis caused by cadmium exposure was demonstrated in this study on a general population environmentally exposed to cadmium in China. It was found that there were significant differences in the prevalence of osteoporosis among the different urinary cadmium groups (chi2 = 18.84, P = 0.0008). The linear trend test gave chi2 = 16.281, P = 0.00005. There was a dose-response relationship between cadmium exposure (urinary cadmium) and prevalence of osteoporosis. Of 31 subjects with osteoporosis, 23 subjects were suffering from renal dysfunction. The prevalence of renal dysfunction (74.19%) was significantly higher than that in those without osteoporosis (chi2 = 16.53, P < 0.001). Stratum analysis was performed to further assess the relationship between bone damage and renal impairment caused by cadmium. There was a significant difference between those with and without tubular damage (chi2 = 19.92, P = 0.000) but not in those with and without glomerular damage (chi2 = 0.08, P = 0.114). This showed that glomerular dysfunction plays a smaller role than tubular dysfunction in the causation of bone damage. It was found that the prevalence of osteoporosis increases with increasing values of parameters of tubular damage. Osteoporosis caused by cadmium is thus related to kidney dysfunction and especially to tubular damage and its severity but not to glomerular damage. The present study has thus demonstrated the combined adverse effects (osteoporosis and renal dysfunction) caused by environmental exposure to cadmium for the first time in Asia outside the endemic area in Japan.

Adult↗
PubMed2004

Lack of reversal effect of EDTA treatment on cadmium induced renal dysfunction: a fourteen-year follow-up.

The aim of this study was to evaluate the effect of ethylenediaminetetraacetic acid (EDTA) on cadmium (Cd) induced renal dysfunction. Seventeen workers (14 males, 3 females) were diagnosed with occupational Cd poisoning in 1986. These individuals had between 7 to 39 years of Cd exposure. From 1986 to 1999, patients received periodic EDTA therapy as part of their follow-up, all at the same hospital. Levels of urinary cadmium (UCd) and urinary beta2-microglobulin (B2M) were measured before and after each annual EDTA treatment period. Renal dysfunction was defined as urinary B2M > 0.8 mg/g Cr (creatinine). In these workers, patients with UCd level higher than 10 microg/g Cr in 1986 had abnormal B2M excretions (> or = 0.8 mg/g Cr) or trended to have abnormal B2M levels during the treatment period. However, in subjects with UCd concentration lower than 10 microg/g Cr in 1986, their urinary B2M excretions either remained normal (< 0.8 mg/g Cr) or returned to normal during the treatment period. The prevalence of renal dysfunction increased during the follow up period regardless of whether UCd levels increased or not, indicating a progressive renal dysfunction despite removal from Cd exposure. Our results suggest that reversibility of renal dysfunction caused by Cd related to the level of Cd exposure at the time of removal from exposure: renal dysfunction could be reversed if initial UCd < 10 microg/g Cr, but was irreversible when UCd > 10 microg/g Cr. Repeated examinations on these 17 Cd exposed workers from 1986 to 1999 also revealed that periodic administration of EDTA had no beneficial effects on chronic Cd-induced renal dysfunction.

Adult↗
PubMed2004

Environmental cadmium exposure and forearm bone density.

Environmental exposure to cadmium may give rise to osteomalacia combined with renal dysfunction, so called 'Itai-Itai disease', which was endemic in the heavily polluted area in Japan. The main focus of this study was to investigate whether environmental exposure to cadmium is associated with low bone mass in a population living near a smelter. A total of 790 persons (302 males and 488 females), who were all over 35 years old and resided in areas near a lead, zinc and cadmium smelter and in a control area in southeast China, completed a questionnaire, and bone mineral density was measured by SPA-4 single photon absorptiometry at the radius and ulna. Cadmium content of urine was determined by graphite-furnace atomic absorption spectrophotometry as a measure of dose. The present study shows that forearm bone densities were negatively correlated with urinary cadmium excretion (p < 0.001) and forearm bone density decreased linearly with age (p < 0.001) and urinary cadmium (p < 0.01), suggesting a dose-effect relationship between cadmium dose and bone mineral density. Based on the World Health Organization criteria, (bone mineral density < -2.5 SDs below the normal young adult), the prevalence of osteoporosis in women increased from 34.0% in the control area to 51.9% in the heavily polluted area (p < 0.01) among subjects over 50 years old, and the odds ratio value was 2.09 (95% CI: 1.08-4.03) for the highly polluted area compared with the control area. A striking observation in the study was a marked increase of the prevalence of fracture in the cadmium-polluted area in both sexes. It was concluded that environmental exposure to cadmium is associated with an increased loss of bone mineral density in both gender, leading to osteoporosis and increased risk of fractures, especially in the elderly and in females.

Adult↗
PubMed2004

Renal dysfunction of cadmium-exposed workers residing in a cadmium-polluted environment.

Human exposure to cadmium may occur in both occupational and general environments. We were interested in determining whether a combination of occupational and environmental exposure to cadmium results in different levels of severity of renal dysfunction relative to that arising from environmental or occupational exposure alone. We selected 44 residents, who once were employed in a smelter and lived in a cadmium-polluted area, as group A. Another 88 subjects, who never worked in the plant, but lived in the same area, were selected as group B. Group C consisted of 88 subjects who had no history of occupational exposure to cadmium and lived in a non-cadmium-polluted area. Statistical analysis demonstrated that there was no significant difference in age or gender among the three groups, nor were there significant differences in smoking habits. The prevalence of renal dysfunction as indicated by increased excretion of beta2-microglobulin (B2M), N-acetyl-beta-D-glucosaminidase (NAG) and albumin (ALB), was higher in group A than in group B. This finding suggests that exposure to cadmium both occupationally and environmentally results in a higher prevalence of renal dysfunction, relative to those who are exposed to cadmium only in the general environment. Therefore, this specific population, who once were occupationally exposed to cadmium and lived in polluted areas, should be identified. Furthermore, health examinations of this population should be conducted in time to prevent further health damage induced by cadmium exposure.

Acetylglucosaminidase↗
PubMed2004

Environmental epidemiological study and estimation of benchmark dose for renal dysfunction in a cadmium-polluted area in China.

We have performed a study aimed at investigating the critical concentration of urinary cadmium (UCd) required for the development of renal dysfunction. We studied population groups (totally 790 persons) living in two cadmium exposed areas and one control area in China. UCd, was determined as an indicator of cadmium exposure and accumulation, while the concentrations of N-acetyl-beta-D-glucosaminidase (NAG), its iso-form B (NAG-B), beta2-microglobulin (B2M), retinol binding protein (RBP), and albumin (ALB) in urine were measured as indicators of the renal effects caused by cadmium. There was a significantly increased prevalence of hyperNAGuria, hyperNAG-Buria, hyperB2Muria, hyperRBPuria and hyperALBuria with increasing levels of Cd excretion in urine. We used the benchmark dose (BMD) procedure to estimate the critical concentration of urinary cadmium in this general population. The lower confidence limit of the BMD (LBMD-05) of urinary cadmium for a 5% level of risk above the background level was estimated for each of the renal effect indicators. The BMD-05/LBMD-05 were estimated to be 4.46/3.99, 6.70/5.87, 8.36/7.31, 7.98/6.98 and 15.06/12.18 microg/g creatinine for urinary NAG-B, NAG, B2M, RBP and ALB, respectively. Our findings suggest, based on the present study, that the Lower Confidence Limit of the Population Critical Concentration of UCd (LPCCUCd-05) of tubular dysfunction for 5% excess risk level above the background may be ca. 3-4 microg/g creatinine, and that cadmium concentration in urine should be kept below this level to prevent renal tubular damage. This report is the first to use the BMD method in this field and to define the concept of critical concentration in urine.

Acetylglucosaminidase↗
PubMed2004

Effects on the prostate of environmental cadmium exposure--a cross-sectional population study in China.

To explore possible effects of environmental cadmium exposure on prostate in humans, and the possible relationship of serum sex hormones to occurrence of clinic signs of tissue changes in the prostate, a case-control study was undertaken in the southeast part of China in 1998. A total of 297 male volunteers from a control area and two cadmium-polluted areas were included as subjects in this study. All the subjects were required to answer a questionnaire and to undergo a complete physical examination including digital-rectal examination (DRE). Blood and urine samples were collected. Serum total prostate specific antigen (PSA), total serum testosterone (T), follicle stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay and enzymeimmunoassay method, respectively. The data of urinary cadmium (U-Cd) and blood cadmium (B-Cd) were obtained by atomic absorption spectrometry (AAS) as an indicator of cadmium body burden. Statistical analysis was applied to investigate a possible relation between cadmium exposure and prostate pathological changes. The results show that there is a clear dose-response relationship between cadmium exposure and the prevalence of cases with abnormal PSA. The blood cadmium content in cases with positive DRE was significantly higher than that of subjects with negative DRE (P < 0.05). Significant differences in the level of FSH between cases with positive DRE and the normal subjects were also noted (P < 0.05). These results indicate that chronic environmental cadmium exposure is associated with injuries to human prostate. A possible relationship to changes in circulating sex hormones needs further investigation.

Adult↗
PubMed2004

Risk assessment on renal dysfunction caused by co-exposure to arsenic and cadmium using benchmark dose calculation in a Chinese population.

Arsenic and cadmium are important inorganic toxicants in the environment. Humans certainly have the potential to be exposed to the mixtures of arsenic and cadmium, but the toxicological interactions of these inorganic mixtures are poorly defined. A general population co-exposed to arsenic and cadmium, was selected in China. The total number of participants was 245, made up of 122 in the arsenic-cadmium polluted area, 123 in the non polluted area. Urinary arsenic (UAs) and cadmium (UCd) were determined by atomic absorption spectrometry as exposure biomarkers and beta2-microglobulin (Ubeta2MG), albumin (UALB), N-acetyl-beta2-glucosaminidase (UNAG) in urine were determined as effect biomarkers. The benchmark dose (BMD) and the lower confidence limit on the benchmark dose (LBMD) were calculated to estimate the critical concentration of UAs and UCd. UAs and UCd concentrations in the polluted area were significantly higher than those in the non polluted area (P < 0.01). The levels of Ubeta2MG, UALB and UNAG in the polluted area were significantly higher than those in the non polluted area (P < 0.01). The BMD/LBMD of UAs and UCd for a 10% level of risk above the background level were estimated as 121.91/102.11 microg/g creatinine and 1.05/0.88 microg/g creatinine. It was suggested that the lower confidence limit of population critical concentration of UAs and UCd for renal dysfunction for 10% excess risk level above the background, which is obtained from LBMD, may need to be kept below 102 and 0.88 microg/g creatinine in order to prevent renal damage in general population co-exposed to arsenic and cadmium. It is indicated that combined effect of arsenic and cadmium were additive effect and/or synergistic effect, and cadmium may potentiate arsenic nephrotoxicity during the long-term and co-exposure to arsenic and cadmium in humans.

Acetylglucosaminidase↗