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Superoxide Dismutase Supplementation

superoxide superoxideradical freeradical dismutase sod melonextract gliadin

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#1 pone11

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Posted 27 December 2014 - 11:21 PM


Superoxide dismutase (SOD) is one of two antioxidants used to neutralize the superoxide radical.   In aerobic metabolism, the electron transport (ETC) chain will produce about 1% to 5% of its energy in the form of destructive free radicals like superoxide.   The ETC lives on the surface of the mitochondrial membrane.   SOD converts the superoxide radical to hydrogen peroxide.   Catalase then acts on the hydrogen peroxide and converts to water and O2.

 

SOD can take two different forms.   The form that uses zinc and copper as its metal resides in the cytoplasm of the cell, outside of the mitochondria.   The form that is used inside the mitochondria uses the metal manganese.

 

SOD is destroyed by digestion, so supplementation has been problematic.   Recently there have been discoveries about how to get SOD past digestion, by encapsulating a particular type of melon extract into a gliadin carrier:

http://www.glisodin.org/glisodin.htm

http://www.plthealth...meline 3-07.pdf

 

This newer type of oral SOD is being marketed as "glisodin" or "SODzyme".

 

See also the section "Natural Ways to Boost SOD Levels" and below in the article:

http://www.lef.org/M...ort_sod/Page-01

 

 

Okay, now with that as background here are my questions:

 

1) Does anyone know whether the SOD found in melon extract is the mitochondrial variety that uses manganese, or is it the cytoplasmic variety that uses zinc / copper?   Because clearly we want the mitochondrial variety.

 

2) Does anyone know whether the rat studies done on glisodin used super high doses to affect systemic SOD levels?   I'm trying to get a sense for whether taking a few SODzymes would really have a material affect on SOD levels in humans.

 

3) Doesn't SOD have a biofeedback mechanism, so if you take a supplement like this every day you get a sharp rise in SOD, followed by a lowering of your endogenous SOD?   If you then quit the supplement weeks later cold-turkey, you will spend a few days in agony as your body has almost zero SOD to deal with any level of oxidative stress.   It takes days for the endogenous SOD to recover.

 

4) Those of us who have wheat intolerance are not thrilled that SODZyme uses gliadin.   Couldn't we accomplish the same thing much more effectively by packaging the SOD in a liposome?  There are recipes online for making liposomal vitamin C, and this kind of home project seems exactly on target to what is done here on Longecity.

 

The main issues for me are:  1) How do we make sure to get the mitochondrial version of SOD;  2) What is proper dosing?  3) Can we ensure sufficient delivery into the mitochondrial matrix, where it would actually be used?


Edited by pone11, 27 December 2014 - 11:29 PM.


#2 sensei

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Posted 28 December 2014 - 04:39 AM

There are 3 forms

 

SOD1 handles ROS within the cytoplasm-- ones that can attack the nucleus and cause damage to nuclear DNA. Said damage can cause early senescence, apoptosis, cross-linkage, or mutation.

 

SOD2 (mn Mitochondrial) Inside the Mitochondria 

 

SOD3 handles extracellular ROS and also contributes an anti-inflammatory action. Inflammation is known to be part of the etiology of atherosclerotic plaques, among other disease states.  Even though it is Cu-Zn like SOD1 -- the enzymatic structure of SOD3 is very different than SOD1

 

SO, no I don't believe that SOD2 (mitochondrial) is the only SOD we need to worry about.

 

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#3 pone11

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Posted 28 December 2014 - 05:17 AM

There are 3 forms

 

SOD1 handles ROS within the cytoplasm-- ones that can attack the nucleus and cause damage to nuclear DNA. Said damage can cause early senescence, apoptosis, cross-linkage, or mutation.

 

SOD2 (mn Mitochondrial) Inside the Mitochondria 

 

SOD3 handles extracellular ROS and also contributes an anti-inflammatory action. Inflammation is known to be part of the etiology of atherosclerotic plaques, among other disease states.  Even though it is Cu-Zn like SOD1 -- the enzymatic structure of SOD3 is very different than SOD1

 

SO, no I don't believe that SOD2 (mitochondrial) is the only SOD we need to worry about.

 

And which of these three SOD types are we getting from the Melon extracts that are being used in SOD supplements?

 

Anyone who knows of good research showing dietary sources for the three types of SOD please publish the references....



#4 sensei

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Posted 28 December 2014 - 05:34 AM

 

There are 3 forms

 

SOD1 handles ROS within the cytoplasm-- ones that can attack the nucleus and cause damage to nuclear DNA. Said damage can cause early senescence, apoptosis, cross-linkage, or mutation.

 

SOD2 (mn Mitochondrial) Inside the Mitochondria 

 

SOD3 handles extracellular ROS and also contributes an anti-inflammatory action. Inflammation is known to be part of the etiology of atherosclerotic plaques, among other disease states.  Even though it is Cu-Zn like SOD1 -- the enzymatic structure of SOD3 is very different than SOD1

 

SO, no I don't believe that SOD2 (mitochondrial) is the only SOD we need to worry about.

 

And which of these three SOD types are we getting from the Melon extracts that are being used in SOD supplements?

 

Anyone who knows of good research showing dietary sources for the three types of SOD please publish the references....

 

According to wikipedia, Fe-SOD (iron), Mn-SOD (manganese) and Cu-Zn-SOD have all been found in higher plants -- some in the same plant just different cells.

 

The issue is that the enzymes are likely not bio-identical to human SOD, bovine Cu-Zn SOD is not molecularly similar to either human versions of Cu-Zn SOD



#5 Kevnzworld

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Posted 28 December 2014 - 06:51 PM

There was a lot of interest and a few clinical studies done with Glisodin almost a decade ago. For whatever reason there wasn't any follow up . LEF markets it in a product called endothelial defense.
I took it for a while, but I've discontinued taking excess antioxidants years ago, this being one of them unless there is further evidence of efficacy.

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#6 pone11

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Posted 28 December 2014 - 09:46 PM

There was a lot of interest and a few clinical studies done with Glisodin almost a decade ago. For whatever reason there wasn't any follow up . LEF markets it in a product called endothelial defense.
I took it for a while, but I've discontinued taking excess antioxidants years ago, this being one of them unless there is further evidence of efficacy.

 

You are afraid that the antioxidants will support cancer growth?

 

In the big picture, we know for sure that we produce a lot of oxidative stress as we age or get sick.   On the other hand, no one really knows if antioxidants increase cancer risk significantly.   If they do, it probably isn't increasing risks more than a few percentage points because they have studied this to death and major anomalies are not showing up in that research.   So for me I have to weigh the certainty of oxidative stress on healthy cells against the - possible - increase of cancer risk by maybe up to 5%.

 

One thing I have wondered about is whether supplementation of any antioxidant that the body produces naturally should be cycled, in order to not too severely dysregulate the body's endogeneous production.   That would imply it might be okay to continually take Vitamin C - which the body cannot produce - but cycle on and off of things like SOD and catalase.







Also tagged with one or more of these keywords: superoxide, superoxideradical, freeradical, dismutase, sod, melonextract, gliadin

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