Apoptosis of peripheral blood mononuclear cells in children exposed to arsenic and fluoride

Rocha-Amador, Diana Olivia; Calderón, Jaqueline; Carrizales, Leticia; Costilla-Salazar, Rogelio; Pérez-Maldonado, Iván N.

doi:10.1016/j.etap.2011.08.004

Cited by 47 publications

(17 citation statements)

References 30 publications

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“…Studies of Mexican children aged 4–13 have reported higher incidences of apoptotic PBMC in As-exposed children relative to controls [64,65]. Although apoptosis is important in immune homeostasis, abnormal immune cell apoptosis can contribute to dysregulated immune function, which may result in immunodeficiency, autoimmune disease or malignant transformation [66]; thus, induced apoptosis may be important in As-mediated immunosuppression.…”

Section: Epidemiological Findingsmentioning

confidence: 99%

“…Although apoptosis is important in immune homeostasis, abnormal immune cell apoptosis can contribute to dysregulated immune function, which may result in immunodeficiency, autoimmune disease or malignant transformation [66]; thus, induced apoptosis may be important in As-mediated immunosuppression. The larger study of 40 children (high and low mean urinary As levels = 46.3 and 14.2 μg/g creatinine, respectively) found a significant positive association between As exposure and apoptotic PBMC [65]. However, despite elevated apoptotic PBMC in chronically-exposed children from the smaller study of 7 highly-exposed and 5 non-exposed children (mean urinary As levels = 143.9 and 24.8 μg/g creatinine, respectively), no significant correlation was observed between exposure and apoptotic cells [64], in agreement with a study on adults [30], possibly due to small sample size or individual differences in As susceptibility [64].…”

Section: Epidemiological Findingsmentioning

confidence: 99%

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Arsenic immunotoxicity: a review

2013

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Exposure to arsenic (As) is a global public health problem because of its association with various cancers and numerous other pathological effects, and millions of people worldwide are exposed to As on a regular basis. Increasing lines of evidence indicate that As may adversely affect the immune system, but its specific effects on immune function are poorly understood. Therefore, we conducted a literature search of non-cancer immune-related effects associated with As exposure and summarized the known immunotoxicological effects of As in humans, animals and in vitro models. Overall, the data show that chronic exposure to As has the potential to impair vital immune responses which could lead to increased risk of infections and chronic diseases, including various cancers. Although animal and in vitro models provide some insight into potential mechanisms of the As-related immunotoxicity observed in human populations, further investigation, particularly in humans, is needed to better understand the relationship between As exposure and the development of disease.

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Section: Epidemiological Findingsmentioning

confidence: 99%

Section: Epidemiological Findingsmentioning

confidence: 99%

Arsenic immunotoxicity: a review

2013

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“…Studies show that arsenic exposure impacts the immune system or alters immune responses in different ways. In humans, experiments show that chronic arsenic exposure causes decrease in T-cell proliferation and cytokine secretion [17], impairment of macrophage functions [18], and increased apoptosis of peripheral blood mononuclear cells [19]. Given the association of arsenic exposure to immunosuppression, hematotoxicity, and associated diseases, one would expect that the immunosuppressive role of arsenic and its metabolites should be evident on the development of the progenitors as well as peripheral lymphoid organ activity.…”

Section: Introductionmentioning

confidence: 99%

Arsenite Selectively Inhibits Mouse Bone Marrow Lymphoid Progenitor Cell Development In Vivo and In Vitro and Suppresses Humoral Immunity In Vivo

et al. 2014

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It is known that exposure to As+3 via drinking water causes a disruption of the immune system and significantly compromises the immune response to infection. The purpose of these studies was to assess the effects of As+3 on bone marrow progenitor cell colony formation and the humoral immune response to a T-dependent antigen response (TDAR) in vivo. In a 30 day drinking water study, mice were exposed to 19, 75, or 300 ppb As+3. There was a decrease in bone marrow cell recovery, but not spleen cell recovery at 300 ppb As+3. In the bone marrow, As+3 altered neither the expression of CD34+ and CD38+ cells, markers of early hematopoietic stem cells, nor CD45−/CD105+, markers of mesenchymal stem cells. Spleen cell surface marker CD45 expression on B cells (CD19+), T cells (CD3+), T helper cells (CD4+) and cytotoxic T cells (CD8+), natural killer (NK+), and macrophages (Mac 1+) were not altered by the 30 day in vivo As+3 exposure. Functional assays of CFU-B colony formation showed significant selective suppression (p<0.05) by 300 ppb As+3 exposure, whereas CFU-GM formation was not altered. The TDAR of the spleen cells was significantly suppressed at 75 and 300 ppb As+3. In vitro studies of the bone marrow revealed a selective suppression of CFU-B by 50 nM As+3 in the absence of apparent cytotoxicity. Monomethylarsonous acid (MMA+3) demonstrated a dose-dependent and selective suppression of CFU-B beginning at 5 nM (p<0.05). MMA+3 suppressed CFU-GM formation at 500 nM, a concentration that proved to be nonspecifically cytotoxic. As+5 did not suppress CFU-B and/or CFU-GM in vitro at concentrations up to 500 nM. Collectively, these results demonstrate that As+3 and likely its metabolite (MMA+3) target lymphoid progenitor cells in mouse bone marrow and mature B and T cell activity in the spleen.

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“…We speculated that this may be related to the cytotoxicity of fluoride. Many studies have shown that the effect of the high concentration of fluoride may cause cell apoptosis, in multiple cell types including hepatocytes [25], human embryo hepatocytes [26], human dental pulp stem cells [27], peripheral blood mononuclear cells [28], and osteoblasts [29]. Thus, we speculated that at higher concentrations of fluoride there may also be induction of B cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Effect of Fluoride on Endocytosis and Surface Marker Expression Levels of Mouse B Cells In Vitro

Shi

Dong

et al. 2016

Cell Physiol Biochem

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Background/Aims: To clarify the effect of fluoride on splenic B cells, the endocytosis and surface marker expression levels of mouse splenic B cells were detected in vitro by flow cytometry. Methods: Cells were stimulated with 10 µg/mL lipopolysaccharide (LPS) and varying concentrations of Sodium Fluoride (NaF) (0, 50 µM, 100 µM, 500 µM, 1000 µM). Results: The results demonstrated that the endocytic capacity of B cells was enhanced by NaF at 50µM. NaF significantly enhanced CD80 expression at 50 µM and decreased CD86 expression at 500 µM. CD40 and CD138 expression on B cells were down-regulated at varying high concentrations of NaF. Conclusion: our results showed that the endocytic capacity, expression levels of CD40 and CD80 of B cells changed significantly at lower concentrations, whereas expression levels of CD138 and CD86 changed significantly at higher concentrations, suggesting that fluoride could inhibit immune function in animals.

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Apoptosis of peripheral blood mononuclear cells in children exposed to arsenic and fluoride

Cited by 47 publications

References 30 publications

Arsenic immunotoxicity: a review

Arsenic immunotoxicity: a review

Arsenite Selectively Inhibits Mouse Bone Marrow Lymphoid Progenitor Cell Development In Vivo and In Vitro and Suppresses Humoral Immunity In Vivo

Effect of Fluoride on Endocytosis and Surface Marker Expression Levels of Mouse B Cells In Vitro

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