Iuval clejan clejan at mindspring.com
Mon Jul 30 17:03:48 EST 2001

Aubrey de Grey wrote:

> To summarise my previous reply: not into the mitochondrial matrix (the
> space enclosed by the inner membrane), but maybe into the intermembrane
> space, where it could indeed be protective.  And it's CuZn, not MnCu.

Yes, thanks. I wish I had a pHD :-) in biology, then I would know how to
spell pH too. Some details matter everywhere in science and engineering, not
just in biology, but some details don't matter that much, like spelling
(unless it's in a grant proposal)..

> > I'm interested in the etiology of higher ploidy in liver cells and one
> > article found that this was weakly inhibited when mice had extra Mn-Cu
> > genes. Is it possible that the Mn-Cu SOD protected mitochondria? Or is
> > this more likely a cytosolic effect?
> I presume you're referring to Nakatani et al, Exp Cell Res 236:137-146.
> (Please get into the habit of including citations when you reference
> published work in postings.)

Right. I'll include references in the future.

> This SOD is highly unlikely to have got
> into the intermembrane space, because it has no targeting sequence.
> (That's not an absolute proof, because the intermembrane space protein
> cytochrome c also has no known targeting sequence, but it's strong
> evidence.)  There is a mention of something that the article calls
> "mitochondrial CuZnSOD",

I didn't see the word "mitochondrial" anywhere. What page?

> but it references a paper (Tsai et al, Biochem
> Int 28:205-217) that I haven't seen, so I wouldn't like to speculate on
> what was actually measured.  I have no more idea than Nakatani et al
> what regulates hepatocyte ploidy, nor whether it is particularly bad
> for us.
> I actually don't see what you're getting at with regard to the role of
> mitochondrial damage (or protection from damage) in this.  Just to make
> sure you understand: the ploidy being discussed is of the nuclear genome,
> not the mtDNA.

Binucleation brought about by acytokinesis seems to be the first step towards
higher ploidy, and it is almost certainly beneficial to some liver functions.
Supposedly it also occurs in cardiac tissue, but I haven't seen these
references. I know that the higher  ploidy here is nuclear, but I have some
reasons to guess (will be posted soon) that nulcear genes involved in
mitochondrial maintanance (which ones are known?) are being replicated to
give an advantage to the mitochondria of the higher ploidy cells.
Your comments are desired...


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