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Manganoporphyrins increase ascorbate-induced cytotoxicity by enhancing H2O2 generation
Journal article   Open access   Peer reviewed

Manganoporphyrins increase ascorbate-induced cytotoxicity by enhancing H2O2 generation

Malvika Rawal, Samuel R Schroeder, Brett A Wagner, Cameron M Cushing, Jessemae Welsh, Anna M Button, Juan Du, Zita A Sibenaller, Garry R Buettner and Joseph J Cullen
Cancer research (Chicago, Ill.), Vol.73(16), pp.5232-5241
08/15/2013
DOI: 10.1158/0008-5472.CAN-13-0470
PMCID: PMC3745518
PMID: 23764544
url
https://doi.org/10.1158/0008-5472.CAN-13-0470View
Published (Version of record) Open Access

Abstract

Renewed interest in using pharmacological ascorbate (AscH − ) to treat cancer has prompted interest in leveraging its cytotoxic mechanism of action. A central feature of AscH − action in cancer cells is its ability to act as an electron donor to O 2 for generating H 2 O 2 . We hypothesized that catalytic manganoporphyrins (MnPs) would increase AscH − oxidation rates, thereby increasing H 2 O 2 fluxes and cytotoxicity. Three different MnPs were tested (MnTBAP, MnT2EPyP, and MnT4MPyP) exhibiting a range of physicochemical and thermodynamic properties. Of the MnPs tested, MnT4MPyP exerted the greatest effect on increasing the rate of AscH − oxidation as determined by the concentration of ascorbate radical [Asc •− ] and the rate of oxygen consumption. At concentrations that had minimal effects alone, combining MnPs and AscH − synergized to decrease clonogenic survival in human pancreatic cancer cells. This cytotoxic effect was reversed by catalase, but not superoxide dismutase, consistent with a mechanism mediated by H 2 O 2 . MnPs increased steady-state concentrations of Asc •− upon ex vivo addition to whole blood obtained either from mice infused with AscH − or patients treated with pharmacologic AscH − . Lastly, tumor growth in vivo was inhibited more effectively by combining MnT4MPyP with AscH − . We concluded that MnPs increase the rate of oxidation of AscH − to leverage H 2 O 2 flux and ascorbate-induced cytotoxicity.

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