Mechanism of selenium-induced inhibition of arsenic-enhanced UVR carcinogenesis in mice.

BACKGROUND: Hairless mice that ingested arsenite in drinking water exhibited more than a 5-fold enhancement of ultraviolet radiation (UVR) carcinogenesis, whereas arsenite alone was carcinogenically inactive. Dietary organoselenium blocked the cancer enhancement effect of arsenic but not cancer indu...

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Publicado en:Environmental Health Perspectives Vol. 116; no. 6; pp. 703 - 709
Autores principales: Burns FJ, Rossman T, Vega K, Uddin A, Vogt S, Lai B, Reeder RJ
Formato: pictorial research tables/charts Journal Article
Publicado: National Institute of Environmental Health Sciences Jun2008
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Jun2008
      vid: 116
      iid: 6
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      pub: National Institute of Environmental Health Sciences
      place: Research Triangle Park, North Carolina
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        10.1289/ehp.10978
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        atl: Mechanism of selenium-induced inhibition of arsenic-enhanced UVR carcinogenesis in mice.
      aug:
        au:
          Burns FJ
          Rossman T
          Vega K
          Uddin A
          Vogt S
          Lai B
          Reeder RJ
        affil: Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York, USA; burns@env.med.nyu.edu
      sug:
        subj:
          Arsenic Adverse Effects
          Carcinogens
          Selenium Pharmacodynamics
          Animal Studies
          Funding Source
          Liver Analysis
          Mice
          Selenium Therapeutic Use
          Skin
          Spectrometry, X-Ray Emission
      ab: BACKGROUND: Hairless mice that ingested arsenite in drinking water exhibited more than a 5-fold enhancement of ultraviolet radiation (UVR) carcinogenesis, whereas arsenite alone was carcinogenically inactive. Dietary organoselenium blocked the cancer enhancement effect of arsenic but not cancer induction by UVR. OBJECTIVE: In this study we sought to explain selenium blockage of As enhancement by establishing the extent that As and Se tissue distributions are coincident or divergent. METHODS: We used the X-ray fluorescence microprobe at the Advanced Photon Source (Argonne National Laboratory) to probe sections of skin and liver from hairless mice exposed to a) UVR, b) UVR + As, c) UVR + organoselenium, or d) UVR + As + organoselenium. RESULTS: We found elevated levels of As in the skin epithelium (hair follicles and epidermis) and diffusely in the liver of mice exposed to UVR + As. Arsenic was entirely absent in skin in mice exposed to UVR + As + organoselenium, but a diffuse low level was seen in the liver. As and Se locations were consistently divergent in skin; As was more diffusely distributed, whereas Se was strongly associated with membranes. X-ray absorption near-edge spectra are consistent with the presence of the seleno-bis(S-glutathionyl) arsinium ion in the liver. CONCLUSIONS: Supplemental Se was uncommonly effective at preventing even a trace of As in skin at 14 or 196 days of continuous exposure to As in drinking water. Traces of the seleno-bis(S-glutathionyl) arsinium ion in the liver suggested that formation of this compound was more likely to be responsible for the As-blocking effect of Se than was a mechanism based on antioxidation.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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