Energy Generation. Each mitochondrion has two separate and specialized membranes. The inner membrane contains the enzymes of the respiratory chain folded into cristae. This encloses a core matrix space that harbors the bulk of certain metabolic enzymes, such as the enzymes of the citric acid cycle. Outside the inner membrane is the intermembrane space, site of ATP synthesis, which is,  in turn, enclosed by the outer membrane; the latter is studded with porin proteins that form aqueous channels permeable to small (<5000 daltons) molecules. Larger molecules (and even some smaller polar species) require specific transporters.
The major source of the energy needed to run all basic cellular functions derives from oxidative metabolism. Mitochondria oxidize substrates to CO2, and in the process transfer high-energy electrons from the original molecule (e.g., gluocse) to molecular oxygen to water. The oxidation of various metabolites drives hydrogen ion (proton) pumps that transfer H+ ions from the core matrix into the inter-membrane space. As these H+ ions flow back down their electrochemical gradient, the energy released is used to synthesize ATP.
It should be noted that the electron transport chain need not necessarily be coupled to ATP generation. Thus, an inner membrane protein enriched in brown fat called thermogenin (or UCP-1 = uncoupling protein 1) is a proton transporter that can dissipate the proton gradient (uncouple it from oxidative phosphorylation) in the form of heat (nonshivering thermogenesis). As a natural (albeit usually low-level) byproduct of substrate oxidation and electron transport, mitochondria also are an important source of reactive oxygen species (e.g., oxygen free radicals, hydrogen peroxide); importantly, hypoxia, toxic injury, or even mitochondrial aging can lead to significantly increased levels of intracellular oxidative stress.
Intermediate Metabolism. Pure oxidative phosphorylation produces abundant ATP, but also “burns” glucose to CO2 and H2O, leaving no carbon moieties for use as building blocks for lipids or proteins. For this reason, rapidly growing cells (both benign and malignant) increase glucose and glutamine uptake and decrease their production of ATP per glucose molecule—forming lactic acid in the presence of adequate oxygen—a phenomenon called the Warburg effect (or aerobic glycolysis). Both glucose and glutamine provide carbon moieties that prime the mitochondrial tricarboxylic acid (TCA) cycle, but instead of being used to make ATP, intermediates are “spun off” to make lipids, nucleic acids, and proteins. Thus, depending on the growth state of the cell, mitochondrial metabolism can be modulated to support either cellular maintenance or cellular growth. Ultimately, growth factors, nutrient supplies, and oxygen availability, as well as cellular signaling pathways and sensors that respond to these exogenous factors, govern these metabolic decisions.
Cell Death. Mitochondria are like the proverbial Dr. Jekyll and Mr. Hyde. On the one hand, they are factories of energy production in the form of ATP that allow the cells to survive; on the other hand, they participate in driving cell death when the cells are exposed to noxious stimuli that the cells cannot adapt to. The role of mitochondria in the two principle forms of cell death, necrosis and apoptosis, are discussed in Chapter 2. In addition to providing ATP and metabolites that enable the bulk of cellular activity, mitochondria also regulate the balance of cell survival and death.