Historically, mitochondria have been thought of as exclusively membrane-bound cell organelles that generate chemical energy needed to power the cell's biochemical reactions. The term mitochondrion was coined by Carl Benda in 1898. However, it was popularly nicknamed the "powerhouse of the cell", by Philip Siekevitz in 1957. Chemical energy produced by mitochondria is stored in the form of adenosine triphosphate (ATP).
Significant new research has found evidence of “mitochondria content” outside of cells. This content exists “as free mtDNA, functional mitochondria or within extracellular vesicles (EVs)”, where it could participate in the etiology of diseases such as cancer or cardiovascular disease. Extracellular mitochondria have been found in plasma and cerebrospinal fluid. What is not clear, though, is whether free mitochondria have always existed or whether they migrate from cells.
Within cells there are ‘quality controls’ that destroy and dispose of damaged or dysfunctional mitochondria that are known to cause cellular damage through reactive oxygen species ROS production. Mitochondrial content that is transferred via EVs is a known phenomena. A transfer of mtDNA has ‘rescued” metabolic activity of recipient cells:
"…mitochondria communicate and collaborate with each other, not only within the same cell but also between different cells, thanks to their ability to come to the rescue of dysfunctional mitochondria that are inside other cells through their release, thus influencing the health of the whole organism.”
Mitochondrial dysfunction has been linked to exposure to certain pharmaceutical drugs especially antimicrobials:
“Bactericidal antibiotics are known to cause oxidative stress and subsequent damage through the disruption of normal mitochondrial functioning. Commonly used antibiotics such as aminoglycosides target both mitochondrial as well as bacterial ribosomes.”