Association of heavy metals and trace elements in carcinoma urinary bladder: A case-controlled study.

Introduction: Abnormal levels of heavy metals (HM) and trace elements (TE) affect body metabolism and can induce carcinogenesis. This study aims to evaluate the role of HM and TE in carcinoma urinary bladder (CAUB). Methods: Patients with biopsy-proven CAUB (n = 100) were taken as the study group, while age-and sex-matched healthy volunteers were taken as control (n = 100). Blood and urine samples were compared for Arsenic (As), Copper (Cu), Manganese (Mn), Selenium (Se), Cadmium (Cd), Lead (Pb), and Mercury (Hg) levels. Serum glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and lipid peroxidation (LPO) levels were assessed to know the redox status between the two groups. Results: A significantly higher blood level of As, Mn, and Pb was observed in CAUB cases as compared to controls. Blood Se level was significantly lower in CAUB patients. On comparing urinary levels, CAUB patients had a higher As, Mn, and Pb levels compared to controls. Further, 68% and 59% of patients had their blood and urinary HM and TE levels above the permitted level, respectively. CAUB cases also had a lower GSH-Px (113.5 ± 44.7 vs. 163.9 ± 120.5, P = 0.0002), lower SOD levels (11.35 ± 5.6 vs. 13.75 ± 3.9, P = 0.008), and a higher LPO levels (15.5 ± 14.7 vs. 11.18 ± 11.2, P = 0.02) in the serum. Conclusions: A significantly higher concentration of As, Mn, and Pb was noted in the blood and urine of CAUB patients compared to controls. CAUB cases also had lower serum GSH-Px and SOD levels with a concomitant increased serum LPO assay suggesting underlying oxidative stress.

Association of heavy metals and trace elements in renal cell carcinoma: A case-controlled study.

PURPOSE: Trace elements and/or heavy metals are important for various biological activities. However, excess amount of these elements is associated with a variety of diseases, including cancer. We aimed to analyse the alterations of trace elements levels in renal cell carcinoma (RCC) patients. MATERIALS AND METHODS: In this observational study, patients with biopsy proven RCC were taken as study group while age- and sex-matched healthy volunteers were taken as control. Blood and urine samples were compared for Arsenic (As), Copper (Cu), Manganese (Mn), Selenium (Se), Cadmium (Cd), Lead (Pb) and Mercury (Hg) levels measured by inductively coupled plasma mass-spectroscopy. Serum glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) antioxidant enzymes and lipid peroxidation (LPO) levels were assessed to know the redox status between 2 groups. RESULTS: A total of 76 RCC cases and 64 controls were recruited in the study. A significantly higher concentration of As, Cu, Mn, Cd, Pb and Hg were observed in the blood of RCC patients as compared to controls. However, blood Se level was significantly lower in RCC patients. In 33 (43.4%) patients, one or more heavy metals were higher in the blood above their permitted level as compared to 10 (15.6%) subjects in control group. RCC patients had a higher urinary Mn and Se levels compared to controls. A significantly lower GSH-Px (182.08 ± 132.91 vs. 236.95 ± 132.94, P = 0.04) and a higher LPO levels (26.02 ± 20.79 vs. 14.06 ± 8.44, P = 0.003) were noted in RCC patients than controls. SOD levels were comparable between two groups. CONCLUSIONS: A significantly altered heavy metals concentration is noted in the blood and urine in RCC patients as compared to healthy controls. An associated lower levels of GSH-Px antioxidant enzyme and increased LPO in RCC patients signifies an imbalance in the redox status.

Quantitative plasma proteomics identifies metallothioneins as a marker of acute-on-chronic liver failure associated acute kidney injury.

Background: Acute kidney injury (AKI) considerably increases the risk of short-term mortality in acute-on-chronic liver failure (ACLF) but predicting AKI is not possible with existing tools. Our study aimed at de novo discovery of AKI biomarkers in ACLF. Methods: This observational study had two phases- (A) Discovery phase in which quantitative proteomics was carried-out with day-of-admission plasma from ACLF patients who initially had no-AKI but either progressed to AKI (n=10) or did not (n=9) within 7 days of admission and, (B) Validation phase in which selected biomarkers from the discovery phase were validated by ELISA in a larger set of ACLF plasma samples (n=93) followed by sub-group analyses. Results: Plasma proteomics revealed 56 differentially expressed proteins in ACLF patients who progressed to AKI vs those who did not. The metallothionein protein-family was upregulated in patients who progressed to AKI and was validated by ELISA as significantly elevated in both- (i) ACLF-AKI vs no-AKI (p-value ≤ 0.0001) and (ii) progression to AKI vs no-progression to AKI (p-value ≤ 0.001). AUROC for AKI vs no-AKI was 0.786 (p-value ≤0.001) and for progression to AKI vs no-progression to AKI was 0.7888 (p-value ≤0.001). Kaplan-Meier analysis revealed that ACLF patients with plasma MT concentration >5.83 ng/mL had a high probability of developing AKI by day 7 (p-value ≤0.0001). High expression of metallothionein genes was found in post-mortem liver biopsies of ACLF patients. Conclusion: Day-of-admission measurements of plasma metallothionein can act as predictive biomarkers of AKI in ACLF.