ABSTRACT
Transition Pore .................................................................................. 272 11.8 Potential Therapeutic Compounds Affecting Mitochondria:
A Mechanistic and Descriptive Approach .................................................... 273 11.9 Certain Classes of Drugs Affecting Mitochondrial Function ...................... 273
11.9.1 Potassium Channel Openers ............................................................. 273 11.9.2 Sulfonylurea Derivatives ................................................................... 274 11.9.3 Ligands of Peripheral Benzodiazepine Receptors ............................ 275 11.9.4 Immunosuppressive Drugs ............................................................... 275 11.9.5 Antiviral Drugs ................................................................................. 276 11.9.6 NSAIDs............................................................................................. 276 11.9.7 Local Anesthetics ............................................................................. 277
The subcellular organelles mitochondria are the prime targets for pharmacological intervention due to their pivotal role in various fundamental metabolic pathways. The malfunctioning of mitochondria may cause or contribute to a large number of human diseases, which include but are not limited to cancer, diabetes, infertility, kidney and liver diseases, and stroke (Modica-Napolitano and Singh 2002; Murphy and Smith 2007; Skulachev et al. 2009; Cunha et al. 2011). The reactive oxygen species (ROS) produced in mitochondria induces mutations and/or defects in mitochondrial DNA (mtDNA) as well as nuclear DNA (Spencer and Sorger 2011). Further, a number of xenobiotics and pharmaceuticals interfere with mitochondrial functions and manifest their toxicity (Wallace and Starkov 2000).
