I'm also concerned about derailing this thread, however...
I was intrigued by post #207 above, which referenced the MitoQ/MitoE/Melatonin study (attached).
So I Googled (well, actually I Bing-ed) MELATONIN and MITOCHONDRIA. There were a lot of hits--many from the early 2000s. But I don't see much discussion of this topic on this forum. (I find a lot on Melatonin and Sleep, Melatonin as a Nootropic, etc..) Am I just missing a major thread, or has this not received much attention?
As the authors of the paper point out, MitoQ is rapidly concentrated in the mitochondria, while Melatonin is widely distributed in the cytoplasm, so they are definitely different beasts. Synergistic? Competitive? This aspect of Melatonin is quite interesting to me, but I don't want to cover the ground again if it has already been thoroughly hashed out previously somewhere on this forum.
I've read about it. Wondered the same thing. If it's as good as MitoQ then it's really good!
Br J Anaesth. 2013 Mar;110(3):472-80. doi: 10.1093/bja/aes577. Epub 2013 Feb 4.Antioxidants that protect mitochondria reduce interleukin-6 and oxidative stress, improve mitochondrial function, and reduce biochemical markers of organ dysfunction in a rat model of acute sepsis.AbstractBACKGROUND:Sepsis-induced organ failure is the major cause of death in critical care units, and is characterized by a massive dysregulated inflammatory response and oxidative stress. We investigated the effects of treatment with antioxidants that protect mitochondria (MitoQ, MitoE, or melatonin) in a rat model of lipopolysaccharide (LPS) plus peptidoglycan (PepG)-induced acute sepsis, characterized by inflammation, mitochondrial dysfunction and early organ damage.
METHODS:Anaesthetized and ventilated rats received an i.v. bolus of LPS and PepG followed by an i.v. infusion of MitoQ, MitoE, melatonin, or saline for 5 h. Organs and blood were then removed for determination of mitochondrial and organ function, oxidative stress, and key cytokines.
RESULTS:MitoQ, MitoE, or melatonin had broadly similar protective effects with improved mitochondrial respiration (P<0.002), reduced oxidative stress (P<0.02), and decreased interleukin-6 levels (P=0.0001). Compared with control rats, antioxidant-treated rats had lower levels of biochemical markers of organ dysfunction, including plasma alanine amino-transferase activity (P=0.02) and creatinine concentrations (P<0.0001).
CONCLUSIONS:Antioxidants that act preferentially in mitochondria reduce mitochondrial damage and organ dysfunction and decrease inflammatory responses in a rat model of acute sepsis.