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Advocacy & Research for Unlimited Lifespans
Posted 27 January 2005 - 09:04 AM
Posted 12 February 2005 - 05:57 PM
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Posted 12 February 2005 - 08:46 PM
Posted 12 February 2005 - 09:54 PM
Posted 12 February 2005 - 10:13 PM
Lynx,
NAC works as a mitochondrial anti-oxidant i.e. it could be used alone with ALCAR without taking any of the above?
Biochemistry. 2004 Jul 6;43(26):8494-502. Related Articles, Links
Modulation of mitochondrial complex I activity by reversible Ca2+ and NADH mediated superoxide anion dependent inhibition.
Sadek HA, Szweda PA, Szweda LI.
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106-4970, USA.
Complex I, a key component of the mitochondrial respiratory chain, exhibits diminished activity as a result of cardiac ischemia/reperfusion. Cardiac ischemia/reperfusion is associated with increases in the levels of mitochondrial Ca(2+) and pro-oxidants. In the current in vitro study, we sought evidence for a mechanistic link between Ca(2+), pro-oxidants, and inhibition of complex I utilizing mitochondria isolated from rat heart. Our results indicate that addition of Ca(2+) to solubilized mitochondria results in loss in complex I activity. Ca(2+) induced a maximum decrease in complex I activity of approximately 35% at low micromolar concentrations over a narrow physiologically relevant pH range. Loss in activity required reducing equivalents in the form of NADH and was not reversed upon addition of EGTA. The antioxidants N-acetylcysteine and superoxide dismutase, but not catalase, prevented inhibition, indicating the involvement of superoxide anion (O2(*-)) in the inactivation process. Importantly, the sulfhydryl reducing agent DTT was capable of fully restoring complex I activity implicating the formation of sulfenic acid and/or disulfide derivatives of cysteine in the inactivation process. Finally, complex I can reactivate endogenously upon Ca(2+) removal if NADH is present and the enzyme is allowed to turnover catalytically. Thus, the present study provides a mechanistic link between three alterations known to occur during cardiac ischemia/reperfusion, mitochondrial Ca(2+) accumulation, free radical production, and complex I inhibition. The reversibility of these processes suggests redox regulation of Ca(2+) handling.
PMID: 15222760 [PubMed - indexed for MEDLINE]
Posted 12 February 2005 - 10:16 PM
does one really need ®-alpha-lipoic acid with ALCAR if you're also taking 3gr Vit C and Theanine as an anti-oxidant ?
Posted 13 February 2005 - 12:46 AM
One thing about NAC is that it is best to use 3:1 Ascorbic Acid/NAC. Ascorbic acid assists in reducing NAC so that it can get back in the battle and also so that it doesn't become a prooxidant.
Posted 13 February 2005 - 12:48 AM
Posted 13 February 2005 - 12:54 AM
Posted 15 February 2005 - 12:01 AM
Posted 15 February 2005 - 12:01 AM
Posted 15 February 2005 - 08:55 PM
Posted 16 February 2005 - 02:28 AM
Posted 08 December 2008 - 05:33 AM
Posted 08 December 2008 - 12:33 PM
does one really need ®-alpha-lipoic acid with ALCAR if you're also taking 3gr Vit C and Theanine as an anti-oxidant ?
Posted 08 December 2008 - 09:18 PM
Posted 08 December 2008 - 10:29 PM
will you provide some literature or information regarding the dangers of ALA at the optimum 60mg/day?
Dietary lipoic acid supplementation can mimic or block the effect of dietary
restriction on life span
Brian J. Merry, Austin J. Kirk, Malcolm H. Goyns
Edited by andre, 08 December 2008 - 10:30 PM.
Posted 09 December 2008 - 07:12 PM
will you provide some literature or information regarding the dangers of ALA at the optimum 60mg/day?
What is particularly worrisome about ALA is that whatever it does to block endogenous adaptations may be effectively permanent, even once you have stopped taking it. The following study discusses such a lifelong side effect with respect to CR, but it is quite possible that it might apply to exercise adaptations and who knows what else:Dietary lipoic acid supplementation can mimic or block the effect of dietary
The human-adjusted effective dose used was about 9g of racemic ALA, which contains 4.5g of R-ALA, but in the absence of dose-ranging studies, it is quite possible that the effect is already significant at your suggested dose of 60mg. There is just no way of knowing at this point.
restriction on life span
Brian J. Merry, Austin J. Kirk, Malcolm H. Goyns
Posted 09 December 2008 - 11:25 PM
Edited by medicineman, 09 December 2008 - 11:27 PM.
Posted 10 December 2008 - 01:26 AM
the maximum dose which no adverse events noted for ala is 60 mg. thats where i got 60mg from.
yea, im gunna research that and provide feedback. oh well. trial and error and education. thats how i dont take vinpo and hup anymore. maybe add another to the list soon.... but not yet..
Posted 10 December 2008 - 09:07 AM
Posted 10 December 2008 - 10:10 PM
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