Arsenic and fluoride co-exposure affects the expression of apoptotic and inflammatory genes and proteins in mononuclear cells from children.
Humans may be exposed to arsenic (As) and fluoride (F) through water consumption. However, the interaction between these two elements and gene expression in apoptosis or inflammatory processes in children has not been thoroughly investigated. Herein, the expression of cIAP-1, XIAP, TNF-α, ENA-78, survivin, CD25, and CD40 was evaluated by RT-PCR. Additionally, the surface expression of CD25, CD40, and CD40L on peripheral blood mononuclear cells was analyzed by flow cytometry, and TNF-α was measured by Western blotting. This study examined 72 children aged 6-12 years who were chronically exposed to As (154.2μg/L) and F (5.3mg/L) in drinking water and in food cooked with the same water. The urine concentrations of As (6.9-122.4μg/L) were positively correlated with the urine concentrations of F (1.0-8.8mg/L) (r(2)=0.413, p<0.0001). The CD25 gene expression levels and urine concentrations of As and F were negatively correlated, though the CD40 expression levels were negatively correlated only with the As concentration. Age and height influenced the expression of cIAP-1, whereas XIAP expression was correlated only with age. Additionally, there was a lower percentage of CD25- and CD40-positive cells in the group of 6- to 8-year-old children exposed to the highest concentrations of both As and F when compared to the 9- to 12-year-old group (CD25: 0.7±0.8 vs. 1.1±0.9, p<0.0014; CD40: 16.0±7.0 vs. 21.8±5.8, p<0.0003). PHA-stimulated lymphocytes did not show any changes in the induction of CD25, CD69, or CD95. In summary, high concentrations of As and F alter the expression patterns of CD25 and CD40 at both the genetic and protein levels. These changes could decrease immune responses in children exposed to As and F.
Laboratory of Immunology and Cellular and Molecular Biology, Faculty of Chemical Sciences, UASLP, Mexico.
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Estrada-Capetillo
Department of Biochemistry, Faculty of Medicine, UASLP, Mexico.
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MD
Ortiz-Pérez
Department of Biochemistry, Faculty of Medicine, UASLP, Mexico.
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Salgado-Bustamante
Department of Toxicology, CINVESTAV, IPN, Mexico.
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Calderón-Aranda
Laboratory of Immunology and Cellular and Molecular Biology, Faculty of Chemical Sciences, UASLP, Mexico.
C J
CJ
Rodríguez-Pinal
Laboratory of Immunology and Cellular and Molecular Biology, Faculty of Chemical Sciences, UASLP, Mexico.
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Reynaga-Hernández
Laboratory of Immunology and Cellular and Molecular Biology, Faculty of Chemical Sciences, UASLP, Mexico.
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Corral-Fernández
Department of Immunology, Faculty of Medicine, UASLP, Mexico.
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González-Amaro
Laboratory of Immunology and Cellular and Molecular Biology, Faculty of Chemical Sciences, UASLP, Mexico. Electronic address: dportale@uaslp.mx.
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Portales-Pérez
D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism; D001151:Arsenic / Q000633:toxicity* / Q000652:urine; D002648:Child; D004781:Environmental Exposure; D005260:Female; D005459:Fluorides / Q000633:toxicity* / Q000652:urine; D015870:Gene Expression / Q000187:drug effects*; D006801:Humans; D007110:Immunity, Active / Q000187:drug effects*; D007249:Inflammation / Q000235:genetics / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000633:toxicity* / Q000652:urine
D051017:Apoptosis Regulatory Proteins; D014409:Tumor Necrosis Factor-alpha; D014874:Water Pollutants, Chemical; D001151:Arsenic; D005459:Fluorides
Arsenic and fluoride co-exposure; Expression of apoptotic and inflammatory genes and proteins; Gene expression; Human cells