Pattern of expression of apoptosis and inflammatory genes in humans exposed to arsenic and/or fluoride

Salgado‐Bustamante, Mariana; Ortiz-Pérez, M. D.; Calderón-Aranda, Emma S.; Estrada-Capetillo, Lizbeth; Niño-Moreno, Perla; González‐Amaro, Roberto; Portales-Pérez, Diana Patricia

doi:10.1016/j.scitotenv.2009.11.016

Cited by 49 publications

(19 citation statements)

References 40 publications

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“…Our data have confi rmed the increasing effect of fl uoride on IL-2, IL-6, and TNF-α levels in rats. In contrast, a recent human ex vivo study revealed lower expression of IL-2 in peripheral blood mononuclear cell obtained from humans exposed to fl uoride (37,38). In our study, however, IL-2 increase following fl uoride intoxication points to immunological response of T cells, as evidenced elsewhere (39).…”

Section: Il-6 = Interleukin-6; Tnf-α = Tumour Necrosis Factor-alpha; contrasting

confidence: 91%

Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

Afolabi

Oyewo

Adekunle

et al. 2013

Archives of Industrial Hygiene and Toxicology

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The aim of this study was to establish the effects of fl uoride on lipid metabolism and attendant infl ammatory response by exposing rats to 50 mg L -1 and 100 mg L -1 of fl uoride through drinking water for seven weeks. Both concentrations led to hypercholesterolemia while the 100 mg L -1 concentration induced hypertriglyceridaemia. High density lipoprotein (HDL) cholesterol levels dropped in the exposed rats while interleukin 2 (IL-2) increased more than 1.5-fold (p<0.05) and IL-6 and plasma TNF-α more than 2.5 fold (p<0.05). Fluoride-exposed rats also had signifi cantly higher levels of liver malondialdehyde (MDA) and plasma lipid hydroperoxide (LOOH) but lower plasma paraoxonase (PON1) activity. Oxidative stress indices correlated with pro-infl ammatory cytokines and plasma cholesterol. In contrast, proinfl ammatory cytokines inversely correlated with plasma triglyceride, HDL cholesterol and PON1. Our results suggest that the association between fl uoride exposure with cardiovascular diseases may be related to its ability to disturb lipid homeostasis, and trigger pro-infl ammatory cytokines and oxidative stress.

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Section: Il-6 = Interleukin-6; Tnf-α = Tumour Necrosis Factor-alpha; contrasting

confidence: 91%

Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

Afolabi

Oyewo

Adekunle

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…More recently, a cDNA microarray study of PBMC from 10 individuals in Mexico having urinary As levels between 117.23 and 435.12 mg/g creatinine ( n = 5) revealed significant differences in expression of apoptosis- and inflammation-related genes compared to unexposed subjects ( n = 5) [22]. Exposure was associated with down-regulated inflammatory genes, including TNF , IL11 , IL10RB , CCR1 , and CXCL2 [22], which is in stark contrast with up-regulated inflammatory genes reported in chronically-exposed persons in Taiwan [21].…”

Section: Epidemiological Findingsmentioning

confidence: 99%

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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“…Using cDNA array test, SalgadoBustamante et al [140] analyzed the expression of approximately 180 genes related to apoptosis and inflammation in peripheral blood mononuclear cells (PBMC) from Mexican human individuals exposed to high fluoride concentration in drinking water. Authors found a significant downregulation of apoptosis-related genes from TNF ligand family (TNFa, FasL, CD30L, CD40L, 4-1BBL, TANK, TRAIL), TNF receptor family (DR3, HVEM), caspase family (Caspase-2, Caspase-6), TRAF family (TRAF-2 and TRAF-5), and CIDE family (CIDE-A and CIDE-B), and upregulation of survivin (BIRC5) from IAP family, which is a regulator of the cellcycle and apoptosis.…”

Section: Gene Expressionmentioning

confidence: 99%

Molecular Mechanisms of Cytotoxicity and Apoptosis Induced by Inorganic Fluoride

2012

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Fluoride (F) is ubiquitous natural substance and widespread industrial pollutant. Although low fluoride concentrations are beneficial for normal tooth and bone development, acute or chronic exposure to high fluoride doses results in adverse health effects. The molecular mechanisms underlying fluoride toxicity are different by nature. Fluoride is able to stimulate G-proteins with subsequent activation of downstream signal transduction pathways such as PKA-, PKC-, PI3-kinase-, Ca 2+ -, and MAPK-dependent systems. G-protein-independent routes include tyrosine phosphorylation and protein phosphatase inhibition. Along with other toxic effects, fluoride was shown to induce oxidative stress leading to excessive generation of ROS, lipid peroxidation, decrease in the GSH/GSSH ratio, and alterations in activities of antioxidant enzymes, as well as to inhibit glycolysis thus causing the depletion of cellular ATP and disturbances in cellular metabolism. Fluoride triggers the disruption of mitochondria outer membrane and release of cytochrome c into cytosol, what activates caspases-9 and -3 (intrinsic) apoptotic pathway. Extrinsic (death receptor) Fas/FasL-caspase-8 and -3 pathway was also described to be implicated in fluoride-induced apoptosis. Fluoride decreases the ratio of antiapoptotic/proapoptotic Bcl-2 family proteins and upregulates the expression of p53 protein. Finally, fluoride changes the expression profile of apoptosis-related genes and causes endoplasmic reticulum stress leading to inhibition of protein synthesis.

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Pattern of expression of apoptosis and inflammatory genes in humans exposed to arsenic and/or fluoride

Cited by 49 publications

References 40 publications

Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

Oxidative Indices Correlate with Dyslipidemia and Pro-Inflammatory Cytokine Levels in Fluoride-Exposed Rats

Arsenic immunotoxicity: a review

Molecular Mechanisms of Cytotoxicity and Apoptosis Induced by Inorganic Fluoride

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