Mitochondria (μίτος, mitos, “thread”, and χονδρίον, chondrion, “granule/grain-like”) are tiny organelles inside most eukaryotic cells which supply cellular energy (by releasing ATP), as well as other functions (cell growth & senescence, differentiation and signalling). Individual mitochondria can vary in size and the number in a cell by organism and cell-type.
There are two hypotheses about the origin of mitochondria: endosymbiotic and autogenous. The endosymbiotic hypothesis suggests that mitochondria were originally prokaryotic cells, capable of implementing oxidative mechanisms that were not possible for eukaryotic cells; they became endosymbionts living inside the eukaryote. In the autogenous hypothesis, mitochondria were born by splitting off a portion of DNA from the nucleus of the eukaryotic cell at the time of divergence with the prokaryotes; this DNA portion would have been enclosed by membranes, which could not be crossed by proteins. Since mitochondria have many features in common with bacteria, the endosymbiotic hypothesis is more widely accepted
Improving mitochondrial functionThere are a few studied ways to improve mitochondrial function:
- Calorific restriction (i.e. intermittent fasting), which in addition to lowering metabolic processes (and therefore making fewer demands on mitochondria) may also "switch on" SIRT1 genes.
- Exercise, which promotes biogenesis -- the production of new mitochondria -- as well as improving the efficiency of existing mitochondria.
- resveratrol, which activates SIRT1 genes - 100-250 mg per day
- L-Carnitine, which shuttles fatty acids to the mitochondria
- D-ribose, which is raw material for ATP molecule
- Omega-3 fatty acids
- B vitamins
Mitochondria, the power plants of the cell, are herds of bacteria-like organelles that bear their own DNA. This DNA becomes damaged in the course of normal cellular processes, and certain forms of mitochondrial DNA damage - to the thirteen genes needed for oxidative phosphorylation - produce malfunctioning mitochondria that can overtake their cells, either by replicating more readily or being more resistant to quality control mechanisms. Such cells become dysfunctional exporters of harmful signals and oxidized proteins, something that contributes to the progression of atherosclerosis via increased amounts of oxidized lipids in the bloodstream, to pick one example. If we're lucky, a substantial proportion of these cells will become senescent as a result of their mutant mitochondria, and will thus be destroyed by senescent cell clearance therapies. Regardless of whether or not that is true, a method of either repairing or working around this type of damage is needed.