Abstract
Health effects elicited by combined environmental exposures to xenobiotics, in many instances, still remain unresolved. One of these examples is the combined toxicity of arsenic and fluoride. The present study was undertaken to delineate the role of inflammation and apoptosis in hepatocellular death caused by co-exposure to arsenic and fluoride in rat. Sodium arsenate (4 mg/kg body weight) and sodium fluoride (4 mg/kg body weight) were administered to female Wistar rats, individually and in combination, for 90 days. Results on tumor necrotic factor-a (TNF-a), interleukin-12 (IL-12), and comet assay showed increased values in comparison to those obtained in arsenic- or fluoride-treated rats. Results on NO, TBARS, and caspase-9 showed higher values than fluoride-treated rats but lower levels than arsenic-treated rats. It is hypothesized that increased generation of nitric oxide induces the release of cytokines that activates caspase-9. Caspase-9 promotes the synthesis of caspase-3 that executes apoptosis. Histopathological observations on apoptotic bodies and Kupffer cells support these observations.
Graphical abstract

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Co-exposure to Arsenic-Fluoride Results in Endoplasmic Reticulum Stress-Induced Apoptosis Through the PERK Signaling Pathway in the Liver of Offspring Rats.
Arsenic and fluoride are two of the major groundwater pollutants. To better understand the liver damage induced during development, 24 male rats exposed to fluoride (F), arsenic (As), and their combination (As + F) from the prenatal stage to 90 days after birth were selected for analysis. Histopathological results showed
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Combined effect of arsenic and fluoride at environmentally relevant concentrations in zebrafish (Danio rerio) brain: Alterations in stress marker and apoptotic gene expression.
Highlights Arsenic and fluoride are the most common hazardous contaminant in the environment. Histological anomalies and alteration of oxidative stress parameters were evident. Stress responsive and apoptotic genes showed less pronounced effects upon co-exposure. DNA ladder was found in both individual treatment, not in combined. Elemental analysis and as3mt
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A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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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-?, ENA-78, survivin, CD25, and CD40 was evaluated by
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Arsenic and fluoride induce neural progenitor cell apoptosis.
The aim of the present study is to determine the effect of inorganic arsenic (As) and its metabolites on the viability of the neural progenitor cell (NPC) line C17.2, in order to evaluate cellular mechanisms involved in As developmental neurotoxicity. Moreover, we analyzed the effects of the coexposure to As
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