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|Title:||Pivotal role of mitochondrial Ca2+ in microcystin-induced mitochondrial permeability transition in rat hepatocytes||Authors:||Ding, W.-X.
Mitochondrial membrane potential
|Issue Date:||2001||Citation:||Ding, W.-X., Shen, H.-M., Ong, C.-N. (2001). Pivotal role of mitochondrial Ca2+ in microcystin-induced mitochondrial permeability transition in rat hepatocytes. Biochemical and Biophysical Research Communications 285 (5) : 1155-1161. ScholarBank@NUS Repository. https://doi.org/10.1006/bbrc.2001.5309||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 Ca2+ in MLR-induced onset of MPT and cell death. Using confocal microscopy, we found that MLR caused an early surge of mitochondrial Ca2+ 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 Ca2+ chelator) or ruthenium red (an inhibitor of mitochondrial Ca2x uniporter) prevented the early mitochondrial Ca2+ 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 mitoehondrial Ca2+ surge, onset of MPT, and cell death. We thus conclude that mitochondrial Ca2+ plays an important role in the onset of MPT and cell death in MLR-treated rat hepatocytes. © 2001 Academic Press.||Source Title:||Biochemical and Biophysical Research Communications||URI:||http://scholarbank.nus.edu.sg/handle/10635/113586||ISSN:||0006291X||DOI:||10.1006/bbrc.2001.5309|
|Appears in Collections:||Staff Publications|
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