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Open AccessJournal ArticleDOI

Inhibition of mitochondria prevents cell death in kidney epithelial cells by intra- and extracellular acidification.

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TLDR
It is concluded that OTA- or cisplatin-induced cell death is dependent on functional and intact, ATP-producing mitochondria and that intra- and extracellular pH is crucial for induction of cell death in IHKE cells.
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This article is published in Kidney International.The article was published on 2003-05-01 and is currently open access. It has received 35 citations till now. The article focuses on the topics: Extracellular & Apoptosis.

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Journal ArticleDOI

Cisplatin Preferentially Binds Mitochondrial DNA and Voltage-Dependent Anion Channel Protein in the Mitochondrial Membrane of Head and Neck Squamous Cell Carcinoma: Possible Role in Apoptosis

TL;DR: Cisplatin binding to nDNA is not necessary for induction of apoptosis in HNSCC, which can result from direct action of cisplatin on mitochondria, which binds preferentially to mitochondrial membrane proteins, particularly the voltage-dependent anion channel.
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p53-dependent caspase-2 activation in mitochondrial release of apoptosis-inducing factor and its role in renal tubular epithelial cell injury.

TL;DR: The role of p53-mediated caspase-2 activation in the mitochondrial release of apoptosis-inducing factor (AIF) in cisplatin-treated renal tubular epithelial cells is demonstrated and caspases and p53 are involved in this release.
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Mitochondria as a critical target of the chemotheraputic agent cisplatin in head and neck cancer.

TL;DR: Recent data have shown that cisplatin may have important direct interactions with mitochondria which can induce apoptosis and may account for a significant portion of the clinical activity associated with this drug.
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Nephrotoxicity of platinum complexes is related to basolateral organic cation transport

TL;DR: It is concluded that cell polarity and basolateral transport mechanisms are essential in nephrotoxicity of platinum drugs.
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Impact of extracellular acidity on the activity of P-glycoprotein and the cytotoxicity of chemotherapeutic drugs.

TL;DR: Data indicate that pGP activity is increased by low extracellular pH presumably as a result of lowered intracellular calcium levels and inhibition of PKC, which may explain the reduced cytotoxicity of chemotherapeutic agents in hypoxic/acidic tumors.
References
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Journal ArticleDOI

On the origin of cancer cells.

Journal ArticleDOI

Mitochondria and apoptosis

TL;DR: A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins.

Origin of cancer cells

Otto Warburg
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Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade

TL;DR: Mutation of the active site of caspase-9 attenuated the activation of cazase-3 and cellular apoptotic response in vivo, indicating that casp enzyme-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and dATP.
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Induction of apoptotic program in cell-free extracts : requirement for datp and cytochrome c

TL;DR: Cells undergoing apoptosis in vivo showed increased release of cy tochrome c to their cytosol, suggesting that mitochondria may function in apoptosis by releasing cytochrome c.
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