51 research outputs found

    Escaping death: Mitochondrial redox homeostasis in cancer cells

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    Reactive oxygen species (ROS) are important signaling molecules that act through the oxidation of nucleic acids, proteins, and lipids. Several hallmarks of cancer, including uncontrolled proliferation, angiogenesis, and genomic instability, are promoted by the increased ROS levels commonly found in tumor cells. To counteract excessive ROS accumulation, oxidative stress, and death, cancer cells tightly regulate ROS levels by enhancing scavenging enzymes, which are dependent on the reducing cofactor nicotinamide adenine dinucleotide phosphate (NADPH). This review focuses on mitochondrial ROS homeostasis with a description of six pathways of NADPH production in mitochondria and a discussion of the possible strategies of pharmacological intervention to selectively eliminate cancer cells by increasing their ROS levels

    Escaping Death: Mitochondrial Redox Homeostasis in Cancer Cells

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    Reactive oxygen species (ROS) are important signaling molecules that act through the oxidation of nucleic acids, proteins, and lipids. Several hallmarks of cancer, including uncontrolled proliferation, angiogenesis, and genomic instability, are promoted by the increased ROS levels commonly found in tumor cells. To counteract excessive ROS accumulation, oxidative stress, and death, cancer cells tightly regulate ROS levels by enhancing scavenging enzymes, which are dependent on the reducing cofactor nicotinamide adenine dinucleotide phosphate (NADPH). This review focuses on mitochondrial ROS homeostasis with a description of six pathways of NADPH production in mitochondria and a discussion of the possible strategies of pharmacological intervention to selectively eliminate cancer cells by increasing their ROS levels

    Aminium salt induced cyclodimerization of stilbenes in 1,1,1,3,3,3-hexafluoropropan-2-ol

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    The aminium salt induced reactions of stilbenes (1a-d), affording a mixture of indane (2a-c) and/or tetra-hydronaphthalene derivatives (3a,c,d), were found to occur with remarkably higher efficiency in 1,1,1,3,3,3-hexafluoropropan-2-ol (HFP) than, if at all, in dichloromethane (DCM) solutions. This solvent effect seems consistent with an electron-transfer mechanism via radical cations 1(+) that chemical evidence indicates to be favoured over an alternative electrophilic mechanism involving carbocations 1H(+), (C) 1999 Elsevier Science Ltd. All rights reserved

    Oxidative activation in aromatic substitutions. Reactions of N,N-dimethylanilines with secondary Anilines promoted by thallium triacetate

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    The reactions of N,N-dimethyl-p-anisidine (1a), N,N-dimethylaniline (1b), and N,N-dimethyl-pfluoroaniline (1c) toward secondary anilines 2(a-d)-H in the presence of thallium triacetate sesquihydrate have been studied as representative of a novel oxidatively activated aromatic substitution affording 1,4-benzenediamine derivatives 3a-d. All of the substrates considered gave substitution with diphenylamine (2d-H). However, with anilines 2b,c-H, only 1a underwent substitution, and substrates 1b,c were practically unreactive. The observed differences in reactivity are well accounted for within a mechanistic framework wherein oxidative activation of both the substrate and the secondary aniline is regarded as alternatively (or simultaneously) possible, depending on the redox characteristics of the reactants. For instance, it can be stated, beyond any reasonable doubt, that reactions of 1a with 2b,c-H proceed via nucleophilic attack of the latter on 1a+¥, and that the reaction of 1a-c with 2d-H must involve the diphenylamino radical 2d¥
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