Display Settings:

Format

Send to:

Choose Destination
    Environ Toxicol Pharmacol. 2009 May;27(3):402-9. Epub 2009 Jan 31.

    Prevention of cadmium-induced toxicity in liver-derived cells by the combination preparation Hepeel(®).

    Source

    Institute of Biochemistry, Medical Faculty, University of Leipzig, Johannisallee 30, 04103 Leipzig, Germany.

    Abstract

    Cadmium is a heavy metal of considerable environmental concern that causes liver damage. This study examined the possible prevention of cadmium toxicity in human HepG2 cells and primary rat hepatocytes by Hepeel(®), a combined preparation of tinctures from seven different plants. Hepeel(®) prevented cadmium chloride (CdCl(2))-induced cell death in both HepG2 cells and hepatocytes, and also reduced the loss of glutathione, lipid peroxidation, nuclear fragmentation, caspase activation and release of mitochondrial cytochrome C. To compare their relative efficacy, the seven constituent plant tinctures of Hepeel(®) were also separately tested. The tinctures China and Nux moschata, which exert solely anti-oxidative effects, failed to reduce cytotoxicity, and only protected against loss of glutathione and lipid peroxidation. In contrast, the tinctures Carduus marianus and Chelidonium, demonstrated anti-apoptotic effects, and protected HepG2 cells and primary hepatocytes against CdCl(2)-induced cell death. These results demonstrate how the effectiveness of Hepeel(®) is determined by the synergistic features of its constituent tinctures. Furthermore, we conclude that cadmium toxicity in the liver is mainly due to stimulation of the intrinsic apoptotic pathway, but may be intensified by increased oxidative stress.

    Copyright © 2009 Elsevier B.V. All rights reserved.

    PMID:
    21783971
    [PubMed - in process]

      Supplemental Content

      Icon for Elsevier Science

      Save items

      loading

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk