Other Parties Interested in Targeting Mitochondria

Amongst plenty of other evidence, I think that the effectiveness of the targeted mitochondrial antioxidant SkQ1 demonstrates handily that the reactive oxygen species generated by your mitochondria are killing you slowly. The damage they cause is a significant portion of aging itself, and targeting mitochondria has become a matter of great interesting to a variety of research groups. The more varied the scientists producing technologies aimed at mitochondria, to more rapidly we are likely to see a good result rapidly. Competition and diversity are real signs of progress soon to come.

I noticed today that the radiology and cancer research community might also have cause to develop means of delivering drugs to mitochondria to alter the output of reactive oxygen species:

Adverse effects of ionizing radiation are mediated through reactive oxygen and nitrogen species. Mitochondria are the principal source of these species in the cell and play an important role in irradiation-induced apoptosis. The use of free radical scavengers and nitric oxide synthase inhibitors has proven to protect normal tissues and, in some cases, to sensitize tumor tissues to radiation damage. Dual molecules that combine radical-scavenging and NOS-inhibitory functions may be particularly effective. Drugging strategies that target mitochondria can enhance the effectiveness of such agents, in comparison to systemic administration, and circumvent side effects.

Which is a good thing. The more the merrier. Still, throwing antioxidants at our mitochondria can only slow down the process of damage. A much better approach is to repair mitochondria that become damaged due to the reactive oxygen species they emit, or change our cells such that the most common forms of mitochondrial damage no longer matter. Both of these are very plausible lines of research, and advances along this road have been demonstrated in the laboratory in recent years:

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