I found this stuff while looking into BHT increasing average lifespan by 45% with talk of slight increases in maximum lifespan.
http://www.lef.org/m...e_harman_01.htm
"...Development of amyloidosis (53-55), and the autoimmune
disorders of NZB and NZB/NZW mice (56), is slowed by antioxidants.
Thus, addition of0. 25% Santoquin to the diet markedly
inhibited amyloid formation in LAF1 male mice, whereas
the same compound increased the average life span ofmale NZB
mice by 32%..."
http://www.pnas.org/...1/7124.full.pdf
I am posting this as a reminder to myself to look into it more and perhaps others might be interested.
Do these anti-oxidants for fats and oils keep the lipids etc in our own bodies from oxidising, preventing arthrosclerosis etc??
Santoquin inhibits amyloid formation; average life extension: 32%
#1
Posted 17 August 2014 - 05:32 PM
#2
Posted 17 August 2014 - 05:58 PM
Ethoxyquin is the real name of this substance; Santoquin
"...Regarding mice, there are a number of antioxidant compounds that will
increase the average life span; for example, 2-mercaptoethylamine [185] and
ethoxyquin [186]. However, there are only three known compounds that have
been shown to increase the maximum life span in mice; they are 2-mercaptoetha-
nol (2-ME) [187], and two pyridine derivatives [188,189]..."
http://plaza.ufl.edu...wen/Pollack.PDF
#3
Posted 17 August 2014 - 06:22 PM
"...Santoquin (ethoxyquin), diphenylamine and N-methylani1ine at a final concentration of 1.0 mM were all effective in preventing the release of the lysosomal hydrolases during the oxidation
of NADPH by liver microsomes. The protection was not due to the inactivation of the lysosomal hydrolases by these substances nor due to the interference with the activities of these three enzymes per se. The addition of Triton X-100 to duplicate systems at the end of the incubation resulted in release of fully active hydrolases. It appears that the oxidation of NADPH by microsomes initiated formation of radicals which, in the presence of Fe2+, attack the lysosomal membrane..."
https://shareok.org/....PDF?sequence=1
Edited by Logic, 17 August 2014 - 06:24 PM.
#4
Posted 17 August 2014 - 08:05 PM
"...Santoquin (ethoxyquin), diphenylamine and N-methylani1ine at a final concentration of 1.0 mM were all effective in preventing the release of the lysosomal hydrolases during the oxidation
of NADPH by liver microsomes. The protection was not due to the inactivation of the lysosomal hydrolases by these substances nor due to the interference with the activities of these three enzymes per se. The addition of Triton X-100 to duplicate systems at the end of the incubation resulted in release of fully active hydrolases. It appears that the oxidation of NADPH by microsomes initiated formation of radicals which, in the presence of Fe2+, attack the lysosomal membrane..."
https://shareok.org/....PDF?sequence=1
One might also consider the reduction of free iron (Fe2+) through depletion of excess/stored iron (bloodletting) and/or sequestration through chelation of free iron with IP6 (Inositol Hexaphosphate) to mimic the effect of Santoquin/ethoxyquin. A cheaper and easier method to the same end?
Iron (& copper)= the ultimate pro-oxidants! Chelate them both with IP6. Give the "over-mineralization theory of aging" a google for more on this.
Edited by synesthesia, 17 August 2014 - 08:11 PM.
Also tagged with one or more of these keywords: santoquin, amyloid, life extension
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