Risk Assessment of Low-Level Cadmium and Arsenic on the Kidney

Abstract

Cadmium (Cd) and arsenic (As) are widely distributed in the environment and are known human carcinogens. Several studies reported that chronic exposure to Cd and As produced renal injuries in humans. As one of the mechanisms, oxidative stress was suggested to play a role in the early process of Cd- and/or As-induced tubular damage in the kidney. This study was performed to evaluate the significance of urinary biomarkers, role of oxidative stress, and effect of coexposure to environmental low-level exposure to Cd and/or As in the general population. Urine samples were collected from 290 adults (86 males and 204 females). Urinary concentrations of Cd and As were measured, and kidney biomarkers of toxicity such as beta(2)-microglobulin and N-acetyl-beta-D-glucosaminidase (NAG) activity determined in urine. Urinary malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels were measured as oxidative stress indices. The mean concentration of Cd was 1.21 microg/L, 0.84 microg/g creatinine, and As was 5.7 microg/L, 3.95 microg/g creatinine in urine. NAG, MDA, and 8-OHdG were positively correlated with both Cd and As in urine. Positive correlations were also observed between NAG and oxidative indices. The effects of coexposure to Cd and As on biomarkers are more pronounced than for exposure to each metal alone. These findings suggest that chronic exposure to low levels of Cd and/or As might produce tubular damage in the kidney through oxidative stress in humans.

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

“…25 It has been monitored in some studies that As increased activities of the oxidant enzymes such as heme oxygenase-1, cyclooxygenase-2 and NADPH that were considered to responsible for the production of arsenic. [30][31][32] ROS leads to oxidation of macromolecules, mainly cell membrane lipids, proteins and DNA. The oxidation of lipids in the cell membrane causes changes in the membrane characteristics and starts a process that leads up to complete loss of the cell.…”

“…Messarah et al 31 have reported that arsenic causes increased level of TBARS, being used in the evaluation of lipid peroxidation, in renal tissue. Huang et al 32 have conducted a study with 290 adults who were exposed to arsenic and reported that levels of MDA and 8-hydroxy-2 0 -deoxyguanosine, used as an indicator of DNA damage, and that urine arsenic level was positively correlated with these indicators. However, there are also studies that have reported that arsenic does not lead to an elevation in the level of lipid peroxidation in renal tissue.…”

Interactions and Mixtures in Metal Toxicology

“…Reproduced from Nordberg et al (2005), with permission from the publisher. endpoints (Huang et al, 2009) also show that coexposure to these elements produced more pronounced effects than with either element alone.…”

Novel and Traditional Cardiovascular Risk Factors in Adolescents

“…Kidney is the key organ to eliminate heavy metals from the body. Heavy metals might lead to albuminuria through inducing oxidative stress to renal tubular cells (118,119). Certain heavy metals have additive effect in inducing nephrotoxicity.…”

“…For example, synergistic effect of arsenic (As) and cadmium (Cd) in causing renal damage has been demonstrated in Chinese general population (120). In addition, chronic exposure to toxic heavy metals may promote atherosclerosis and contribute to the development of chronic kidney disease and cardiovascular diseases (119,121). Furthermore, air pollutants can provoke systemic proinflammatory and pro-thrombotic response and lead to increase in platelet counts and platelet activation (122).…”