These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Disturbance of voltage-induced cellular calcium entry by marine dimeric and tetrameric pyrrole--imidazole alkaloids.
    Author: Bickmeyer U, Grube A, Klings KW, Köck M.
    Journal: Toxicon; 2007 Sep 15; 50(4):490-7. PubMed ID: 17570456.
    Abstract:
    Twelve brominated pyrrole-imidazole alkaloids from the Caribbean sponges Stylissa caribica and Agelas wiedenmayeri were tested for interactions with cellular calcium homeostasis using PC12 cells. Massadine (half maximal concentration: 5.32 +/- 0.007microM), stylissadines A (4.48 +/- 1.1microM) and B (4.6 +/- 1.6microM) as well as tetrabromostyloguanidine (15.6 +/- 0.004microM) reduced voltage-dependent calcium entry in PC12 cells as measured with Fura II as calcium indicator. Dibromopalau'amine and mauritiamine reduced voltage-dependent calcium entry but no half maximal concentration can be calculated from our results. Monomeric brominated pyrrole alkaloids such as stevensine, cyclooroidin, oxocyclostylidol, 4-bromopyrrole-2-carboxy-N(epsilon)-lysine, and 4-bromopyrrole-2-carboxyarginine showed no or only minor effects. Ageladine A itself showed fluorescence in a similar range as Fura II and therefore no data are reported here. Based on the results a structure-activity relationship could be established. Absolutely necessary for an activity seem to be a lipophilic (brominated side chain) and a hydrophilic (amino-imidazole core) substructure. The combination of these substructures may be on one hand responsible for the membrane solubility (dibromopyrrole moieties) and on the other hand for the interaction with the hydrophilic area of the calcium channel (amino-imidazole moieties) to accomplish the alkaloids neurotoxic potential.
    [Abstract] [Full Text] [Related] [New Search]