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: Pivotal role of mitochondrial Ca(2+) in microcystin-induced mitochondrial permeability transition in rat hepatocytes.
    Author: Ding WX, Shen HM, Ong CN.
    Journal: Biochem Biophys Res Commun; 2001 Aug 03; 285(5):1155-61. PubMed ID: 11478775.
    Abstract:
    We have shown earlier that microcystin-LR (MLR), a specific hepatotoxin, induced onset of mitochondrial permeability transition (MPT) and apoptosis in rat hepatocytes. Here we attempted to investigate the role of mitochondrial Ca(2+) in MLR-induced onset of MPT and cell death. Using confocal microscopy, we found that MLR caused an early surge of mitochondrial Ca(2+) prior to the onset of MPT and cell death. Pretreatment with 1,2-bis(O-aminophenoxyl)ethane-N,N,N',N'-tetracetic acid tetra(acetoxymethyl)ester (an intracellular Ca(2+) chelator) or ruthenium red (an inhibitor of mitochondrial Ca(2+) uniporter) prevented the early mitochondrial Ca(2+) surge and attenuated the subsequent onset of MPT and cell death. On the other hand, a mitochondrial uncoupler, CCCP, rapidly disrupted the mitochondrial membrane potential and also prevented the mitochondrial Ca(2+) surge, onset of MPT, and cell death. We thus conclude that mitochondrial Ca(2+) plays an important role in the onset of MPT and cell death in MLR-treated rat hepatocytes.
    [Abstract] [Full Text] [Related] [New Search]