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-α (TNF-α), 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.
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Authors | Huma Khan, Yeshvandra Verma, S V S Rana |
Journal | Biological trace element research
(Biol Trace Elem Res)
Vol. 200
Issue 7
Pg. 3227-3235
(Jul 2022)
ISSN: 1559-0720 [Electronic] United States |
PMID | 34850329
(Publication Type: Journal Article)
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Copyright | © 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. |
Chemical References |
- Caspase 9
- Arsenic
- Fluorides
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Topics |
- Animals
- Apoptosis
- Arsenic
(metabolism)
- Body Weight
- Carcinoma, Hepatocellular
- Caspase 9
- Female
- Fluorides
(toxicity)
- Inflammation
(chemically induced)
- Liver Neoplasms
- Oxidative Stress
- Rats
- Rats, Wistar
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