Pyrroloquinoline Quinone and Mitochondria
Control of mitochondrial oxygen utilization and respiratory control is central to all aspects of normal growth and development. In a broad setting, mitochondria are central to normal glucose, amino acid and fatty acid oxidation, reactive oxygen species (ROS), i.e., antioxidant modulation, and ATP production, particularly during exercise. The mechanisms for mitochondrial regulation involve changes in the number of mitochondria per cell, the assembly and disassembly of mitochondria, control of transport of substances into and out of mitochondria, as well as control on the levels of activity of mitochondrial-related enzymes. Indeed, the importance of mitochondria to energy regulation cannot be understated. Mitochondria generate most of the cell’s supply of ATP, which is the major source of a cell’s potential chemical energy.
Moreover, in addition to supplying cellular energy, mitochondria are also important to cellular regulatory signaling, and the eventual programmed cell death (or apoptosis) and turnover of cells. The lifespan of all cells is directly linked to mitochondrial assembly and production. Such events can control new tissue growth, the response to infections, and nerve cell signaling and control. In the average adult, between 50 and 70 billion cells turnover each day due to apoptosis pr programmed cell death. In a year, this can amount to the proliferation and subsequent destruction of a mass of cells equal to one’s body weight! When mitochondrial function at any level is compromised there can be a number of metabolic and health-related metabolic consequences. Examples are a decline in mitochondrial oxidative efficiency, which is thought to be a major underlying feature of the metabolic syndromes that can lead to increased blood pressure and lipid levels, poorer responses to inflammation and, when targeted and severe, neurological disorders, such as Parkinson’s disease and Alzheimer’s dementia.