by Biologist » Wed Mar 12, 2008 11:17 pm
OK, I'll take a shot at it now:
"...they refer to an 'inherited' eye problem that is the
result of compromised CoQ10. Did you understand
that?"
--Brooks
An *inherited* mitochondrial mutation, which generally implies that ALL the mitochondrial units in every cell of the body are effected, will show the most pathology in tissues and organs where ATP demand is highest -- such as for the optic nerves. There's a huge demand there! The specific type of mutation they cite apparently has to do with compromised DNA instructions for the construction of a part (i.e., a subunit) of a particular mitochondrial protein, the NADH-C0Q reductase enzyme. The loss of that enzyme (or is impaired function, limiting ATP production) shows up most spectacularly in the optic nerve due to very high power demands there, but we can be sure it impairs many other organs and systems throughout the body as well. Note that we do not face inherited mitochondrial mutations, but rather impaired mitochondria function of various types and origins -- Beatup Mitochondria Syndrome (to coin a term). Some of these defects may involve *acquired* mutations to the mitochondrial DNA of some units (such that daughter cells will replicate the error); but some of the defects may be correctable with improved conditions (e.g., improved cellular carnitine availability) such that the unit can get back on its feet again and its future division will be fine; and of course, some are so screwed up they just die, which is OK, as there are so many of them in each cell which can be replaced by good ones dividing. Most of our bodies' hundreds of trillions of mitochondria are fine or have limited damage that is not passed on to daughter cells. (BTW, note the comment that kids can survive fine with only 15% of mitochondrial units functioning.) I suspect we are much are better off than those with serious "global loss" from any particular mitochondrial mutation that consistently precludes the production of particular proteins for optimal function in all mitochondrial units such as in the disease they cite.
"I was not able to find out exactly HOW antibiotics
interact with Statin drugs; what the physical result
is... did you find that?"
--Brooks
The antibiotic provides the "additional insult" of selectively knocking out a mitochondrion's ability to produce one of more of the very few vital proteins that it makes (i.e, codes for and constructs) on-site to maintain and repair itself. It blocks production. Such a temporary impairment of protein production due to a course of antibiotics is survivable to a healthy mitochondrial unit, but not one screwed up by statins. There appears to be a synergism of impairment created by the two that pushes the unit over the edge -- to either death or permanent or semi-permanent dysfunction. It's like the Enterprise taking a Klingon photon torpedoe (the antibiotic) while the shields are down (due to statins).
Biologist