Background: The mitochondria may very well determine the final commitment of the
cell to death, particularly in times of energy stress. Cancer chemotherapeutics such as the anthracycline
doxorubicin perturb mitochondrial structure and function in tumour cells, as evidenced in osteosarcoma,
for which doxorubicin is used clinically as frontline therapy. This same mechanism of
cell inhibition is also pertinent to doxorubicin’s primary cause of side-effects, that to the cardiac tissue,
culminating in such dire events as congestive heart failure. Reactive oxygen species are partly
to blame for this effect on the mitochondria, which impact the electron transport chain.
Objective: As this review highlights that, there is much more to be learnt about the mitochondria and
how it is affected by such effective but toxic drugs as doxorubicin.
Conclusion: Such information will aid researchers who search for cancer treatment able to preserve
mitochondrial number and function in normal cells.