Talk:Mitochondrion: Difference between revisions
imported>David E. Volk mNo edit summary |
imported>John Stephenson (→High priority: Any idea why this page is so popular?) |
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== High priority == | == High priority == | ||
This is a high priority Google search item--don't ask me why, we don't have an article about it yet! --[[User:Larry Sanger|Larry Sanger]] 16:58, 11 October 2007 (CDT) | This is a high priority Google search item--don't ask me why, we don't have an article about it yet! --[[User:Larry Sanger|Larry Sanger]] 16:58, 11 October 2007 (CDT) | ||
:This is the third-most popular page on CZ according to [[Special:PopularPages]]. I wonder why? [[User:John Stephenson|John Stephenson]] 10:47, 22 September 2010 (UTC) | |||
== About "Neurotoxicity and neuroprotection"== | |||
I think that the processes of necrosis and apoptosis involve free radical generation catalyzed by Ca++ (calcification of the mitochondrion). If I understood well, Ca++ in mitochondria behaves like Fe++ and Cu++ out of mitochondria: it catalyzes [[Fenton reaction]]s. | |||
Perhaps we could determine whether all this is restricted to ''neuronal'' mitochondria, or if all mitochondria eventually follow the same pathological/senescent course. | |||
[[User:Pierre-Alain Gouanvic|Pierre-Alain Gouanvic]] 01:43, 2 February 2008 (CST) | |||
==Updated external links== | |||
As you know from time to time external links expire. I have just ascertained that all external links in this article are still functioning and there is no current dead link. [[User:Thomas Simmons|Thomas Simmons]] 20:49, 14 January 2009 (UTC) | |||
Latest revision as of 04:47, 22 September 2010
High priority
This is a high priority Google search item--don't ask me why, we don't have an article about it yet! --Larry Sanger 16:58, 11 October 2007 (CDT)
- This is the third-most popular page on CZ according to Special:PopularPages. I wonder why? John Stephenson 10:47, 22 September 2010 (UTC)
About "Neurotoxicity and neuroprotection"
I think that the processes of necrosis and apoptosis involve free radical generation catalyzed by Ca++ (calcification of the mitochondrion). If I understood well, Ca++ in mitochondria behaves like Fe++ and Cu++ out of mitochondria: it catalyzes Fenton reactions.
Perhaps we could determine whether all this is restricted to neuronal mitochondria, or if all mitochondria eventually follow the same pathological/senescent course.
Pierre-Alain Gouanvic 01:43, 2 February 2008 (CST)
Updated external links
As you know from time to time external links expire. I have just ascertained that all external links in this article are still functioning and there is no current dead link. Thomas Simmons 20:49, 14 January 2009 (UTC)