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Appendix 2. Direct and Indirect Inhibitors of Mitochondrial ATP Synthesis
APPENDIX 2
Direct and Indirect Inhibitors of Mitochondrial ATP Synthesis Nanette Orme-Johnson Department of Biochemistry, Tufts University School of Medicine Boston, Massachusetts 02111
A few important notes about the tables in this appendix. The information in the tables is in no sense complete with respect to the compounds listed or the references cited for their use. I have tried to include the more commonly used inhibitors and others that are of either historical interest or that have been found recently and may become more widely used. The frequency of use of a compound may be assessed by the number of references indicated, that is, *(fewer than 10 references), **(10–100 references), or ***(greater than 100 references). Additionally, when possible, I have tried to cite mainly recent references, thus, if the latest reference for a compound is, for example, 1975, you may conclude that this compound is probably not used frequently now. I have also tried to cite papers using a given inhibitor in a number of experimental settings, for example, tissue or cells (T/C), whole mitochondria (M), and so on. This is intended to indicate the concentration of inhibitor that will cause the eVect in that context. An interesting review by Wallace (1) on mitochondria as targets of drug toxicity considers how the drugs inhibit various reactions needed for the synthesis of ATP. I have not considered here compounds, for example, many of the HIV therapeutic drugs (2), that decrease mitochondrial ATP production indirectly by inhibiting the synthesis of mitochondrial DNA thus reducing the levels of proteins needed for ATP synthesis.
METHODS IN CELL BIOLOGY, VOL. 80 Copyright 2007, Elsevier Inc. All rights reserved.
813
0091-679X/07 $35.00 DOI: 10.1016/S0091-679X(06)80041-5
Direct and Indirect Inhibitors of Mitochondrial ATP Synthesis Nanette Orme-Johnson Department of Biochemistry, Tufts University School of Medicine Boston, Massachusetts 02111
A few important notes about the tables in this appendix. The information in the tables is in no sense complete with respect to the compounds listed or the references cited for their use. I have tried to include the more commonly used inhibitors and others that are of either historical interest or that have been found recently and may become more widely used. The frequency of use of a compound may be assessed by the number of references indicated, that is, *(fewer than 10 references), **(10–100 references), or ***(greater than 100 references). Additionally, when possible, I have tried to cite mainly recent references, thus, if the latest reference for a compound is, for example, 1975, you may conclude that this compound is probably not used frequently now. I have also tried to cite papers using a given inhibitor in a number of experimental settings, for example, tissue or cells (T/C), whole mitochondria (M), and so on. This is intended to indicate the concentration of inhibitor that will cause the eVect in that context. An interesting review by Wallace (1) on mitochondria as targets of drug toxicity considers how the drugs inhibit various reactions needed for the synthesis of ATP. I have not considered here compounds, for example, many of the HIV therapeutic drugs (2), that decrease mitochondrial ATP production indirectly by inhibiting the synthesis of mitochondrial DNA thus reducing the levels of proteins needed for ATP synthesis.
METHODS IN CELL BIOLOGY, VOL. 80 Copyright 2007, Elsevier Inc. All rights reserved.
813
0091-679X/07 $35.00 DOI: 10.1016/S0091-679X(06)80041-5