ABSTRACT
BACKGROUND: Exposure to lead (Pb) in environmental and occupational settings continues to be a serious public health problem and may pose an elevated risk of genetic damage. OBJECTIVES: The aim of this study was to assess the level of oxidative stress and DNA damage in subjects occupationally exposed to lead. MATERIAL AND METHODS: We studied a population of 78 male workers exposed to lead in a lead and zinc smelter and battery recycling plant and 38 men from a control group. Blood lead levels were detected by graphite furnace atomic absorption spectrophotometry and plasma lead levels by inductively coupled plasma-mass spectrometry. The following assays were performed to assess the DNA damage and oxidative stress: comet assay, determination of 8-hydroxy-2'-deoxyguanosine (8-OHdG), lipid peroxidation and total antioxidant status (TAS). RESULTS: The mean concentration of lead in the blood of the exposed group was 392 ± 103 µg/L and was significantly higher than in the control group (30.3 ± 29.4 µg/L, p < 0.0001). Oxidative DNA damages measured by comet assay showed no significant differences between populations. The concentration of 8-OHdG was about twice as high as in the control group. We found a significant positive correlation between the level of biomarkers of lead exposure [lead in blood, lead in plasma, zinc protoporphyrin (ZPP)] and urine concentration of 8-OHdG. The level of oxidative damage of DNA was positively correlated with the level of lipid peroxidation (TBARS) and negatively with total anti-oxidative status (TAS). CONCLUSIONS: Our study suggests that occupational exposure causes an increase in oxidative damage to DNA, even in subjects with relatively short length of service (average length of about 10 years). 8-OHdG concentration in the urine proved to be a sensitive and non-invasive marker of lead induced genotoxic damage.
Subject(s)
DNA Damage , Lead/adverse effects , Occupational Exposure/adverse effects , Occupational Health , Oxidative Stress/drug effects , 8-Hydroxy-2'-Deoxyguanosine , Adult , Antioxidants/metabolism , Biomarkers/blood , Biomarkers/urine , Case-Control Studies , Comet Assay , Deoxyguanosine/analogs & derivatives , Deoxyguanosine/urine , Electric Power Supplies , Humans , Job Description , Lead/blood , Lipid Peroxidation/drug effects , Male , Mass Spectrometry/methods , Middle Aged , Recycling , Time Factors , Urinalysis , Welding , Young AdultABSTRACT
The aim of this study was to assess the effects of chronic combined exposure to low, environmental doses of Cd, Pb, and Mn on oxidative stress in the liver and heart of rats and on their liver function parameters. Male Wistar rats were divided randomly into eight groups. For nine months controls were receiving drinking water alone, whereas the exposed groups were receiving drinking water with Pb (0.2 mg L(-1)), Cd (1 mg L(-1)), and Mn (2 mg L(-1)) alone or in combinations. Malondialdehyde (MDA) significantly increased in both heart and liver of the animals after combined exposure to metals. Heart MDA correlated with blood Cd, Pb, and Mn and liver MDA with blood Cd. Aspartate aminotransferase (AST) activity and bilirubin concentration also increased significantly in the animal group exposed to all three metals and correlated positively with blood Cd, Pb, and Mn. Our study has confirmed the synergistic effect of the Cd, Mn, and Pb combination on the increase in heart MDA. A similar synergy was observed for Pb+Mn in the increase of serum alanine aminotransferase (ALT) activity as an indicator of liver function.
