The Level of Selenium and Oxidative Stress in Workers Chronically Exposed to Lead.

The possible beneficial role of selenium (Se) on the oxidative stress induced by lead (Pb) is still unclear in humans. Therefore, the aim of the present study was to explore the associations among the Se levels, chronic Pb exposure, oxidative stress parameters, and parameters characterizing the function of the antioxidant defense system in men who are occupationally exposed to Pb. Based on the median serum Se concentrations, the 324 study subjects were divided into two subgroups: a subgroup with a low Se level (L-Se) and a subgroup with a high Se level (H-Se). The levels of lead (PbB) and zinc protoporphyrin (ZPP) in the blood and the delta-aminolevulinic acid (ALA) level in the urine served as indices of Pb exposure. The PbB level was significantly lower in the H-Se group compared to that in the L-Se group by 6 %. The levels of 8-hydroxyguanosine and lipofuscin (LPS) and the activity of superoxide dismutase were significantly lower in the H-Se group compared to that in the L-Se group by 17, 19, and 11 %, respectively. However, the glutathione level (GSH) and the activities of glutathione peroxidase (GPx) and catalase were significantly higher by 9, 23, and 3 %. Spearman correlations showed positive associations between the Se level and GPx activity and GSH level. A lower serum Se level in chronically Pb-exposed subjects is associated with higher Pb blood levels and an elevated erythrocyte LPS level, which reflects the intensity of oxidative stress. Besides, in a group of Pb-exposed subjects with lower serum Se level, depleted GSH pool and decreased activity of GPx in erythrocytes were reported. However, the present results are inadequate to recommend Se supplementation for chronic lead exposure at higher doses than would be included in a normal diet except for selenium deficiency.

Telomere length, telomerase expression, and oxidative stress in lead smelters.

The negative health effects caused by lead (Pb) exposure are widely recognized; however, the molecular mechanisms remain unknown. The aim of this study was to assess the effect of occupational Pb exposure on telomere length and to investigate the potential mechanisms leading to telomere shortening. A cohort of 334 male Pb smelters (exposed group) and 60 age-adjusted males unexposed to Pb (control group) were examined. Assessments of relative telomere length (rTL) and telomerase reverse transcriptase (TERT) gene expression were performed using quantitative real-time polymerase chain reactions. Assessments of whole blood Pb (B-Pb) and whole blood cadmium (B-Cd) concentrations and serum selenium concentration (S-Se) were performed using graphite furnace atomic absorption spectrometry. We analyzed total oxidation status (TOS), lipid hydroperoxides (LHPs), malonylodialdehyde levels in serum (MDA) and in erythrocyte hemolysates (MDA-hgb), and 8-hydroxy-deoxy-guanosine (8-OHdG). The Pb-exposed group had higher B-Pb values and shorter rTL than the control group. The arithmetic mean values calculated for B-Pb were 33 µg/dL versus 2.2 µg/dL (p < 0.0001), and the rTL values were 0.928 and 1.126 relative units (p = 0.001), respectively, for the Pb-exposed and control groups. The rTL was found to gradually shorten in response to the increasing levels of Pb exposure. The Pb-exposed group also demonstrated a higher level of oxidative stress than the control group, which was indicated by increased TOS and MDA-hgb values. rTL was negatively associated with parameters that indicated increased oxidative stress, including TOS (Spearman's rank coefficient (rS) = -0.16; p < 0.01) and MDA-hgb (rS = -0.17; p < 0.001). No correlations were found between rTL and B-Cd and S-Se or smoking and MDA and LHP levels. Univariate analysis indicated that B-Pb was associated with decreased rTL (ß =-0.0041; p = 0.0063) and that the association between B-Pb and rTL remained significant, even when adjusting for age (ß = -0.0041; p = 0.0065) and in multivariable-adjusted model (ß = -0.0042; p = 0.0063). In conclusion, occupational Pb exposure resulted in decreased rTL and may represent a mechanism that contributes to Pb-related diseases.