Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2569925 | Toxicology and Applied Pharmacology | 2010 | 8 Pages |
Abstract
Arsenic (As) exposure has been associated with alterations in the immune system, studies in experimental models and adults have shown that these effects involve macrophage function; however, limited information is available on what type of effects could be induced in children. The aim of this study was to evaluate effects of As exposure, through the association of inorganic As (iAs) and its metabolites [monomethylated arsenic (MMA) and dimethylated arsenic (DMA)] with basal levels of nitric oxide (NOâ) and superoxide anion (O2â), in peripheral blood mononuclear cells (PBMC) and monocytes, and NOâ and O2â produced by activated monocytes. Hence, a cross-sectional study was conducted in 87 children (6-10 years old) who had been environmentally exposed to As through drinking water. Levels of urinary As species (iAs, MMA and DMA) were determined by hydride generation atomic absorption spectrometry, total As (tAs) represents the sum of iAs and its species; tAs urine levels ranged from 12.3 to 1411 μg/g creatinine. Using multiple linear regression models, iAs presented a positive and statistical association with basal NOâ in PBMC (β = 0.0048, p = 0.049) and monocytes (β = 0.0044, p = 0.044), while basal O2â had a significant positive association with DMA (β = 0.0025, p = 0.046). In activated monocytes, O2â showed a statistical and positive association with iAs (β = 0.0108, p = 0.023), MMA (β = 0.0066, p = 0.022), DMA (β = 0.0018, p = 0.015), and tAs (β = 0.0013, p = 0.015). We conclude that As exposure in the studied children was positively associated with basal levels of NOâ and O2â in PBMC and monocytes, suggesting that As induces oxidative stress in circulating blood cells. Additionally, this study showed a positive association of O2â production with iAs and its metabolites in stimulated monocytes, supporting previous data that suggests that these cells, and particularly the O2â activation pathway, are relevant targets for As toxicity.
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Authors
Ana L. Luna, Leonor C. Acosta-Saavedra, Lizbeth Lopez-Carrillo, Patricia Conde, Eunice Vera, Andrea De Vizcaya-Ruiz, Mariana Bastida, Mariano E. Cebrian, Emma S. Calderon-Aranda,