Poly-unsaturated fatty acids & Lipid peroxidation

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Poly-unsaturated fatty acids & Lipid peroxidation

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Poly-unsaturated fatty acids (PUFAs)

PUFAs contain more than one double bond in their backbone.
PUFAs include omega-3, omega-6 and omega-9 fatty acids.
20% of the dry weight of the brain is made up of PUFAs and
33% of fatty acids in the central nervous system (CNS) are PUFAs.Bourre JM
Most of the PUFAs ingested from foods are essential fatty acids.

Essential fatty acids; those that are required for biological purposes other than fuel,
and cannot be produced by the human body.
- alpha-linolenic acid (ALA; omega-3 fatty acid)
- linoleic acid (LA; omega-6); is the main PUFA in mammals.Spiteller G
Though it is proposed that AA and DHA are the true essential fatty acids Le HD et al,
which need to be in balance, at least during brain development.van Goor LA et al

PUFAs also include semi-essential fatty acids; those that are required for biological purposes other than fuel,
and (conditionally) may not be sufficiently produced by the human body.
- eicosapentaenoic acid (EPA; omega-3)
- docosapentaenoic acid (DPA; omega-3)
- docosahexaenoic acid (DHA; omega-3)

- gamma-linolenic acid (GLA; omega-6)
- dihomo-gamma-linolenic acid (DGLA; omega-6)
- arachidonic acid (AA; omega-6)


Biological functions

In human breast milk, up to 2% of total fat is long-chain PUFA Gil A et al

Omega-3 fatty acids play a critical role in the development and function of the central nervous system.Logan AC
Omega-3 fatty acids are an essential component of CNS membrane phospholipid acyl chains, critical to the dynamic structure and function of neuronal membranes.Bourre JM et al
Omega-3 fatty acids are important physiological regulators of energy metabolism and overall energy homeostasis.Panickar KS et al
Omega-3 fatty acids positively affect pre-natal neurodevelopment. At later ages, multiple studies found evidence suggesting that n-3 PUFA can protect against neurodegeneration and possibly reduce the chance of developing cognitive impairment.Karr JE et al
Omega-3 deficiency during the perinatal period may cause increased blood pressure later in life.Armitage JL Effects in adults are small Cabo J et al
Omega-3 fatty acid supplementation reduces amyloid-β in animal models of AD, also improving cognitive function, and in female animals diminishes neuronal loss.Hooijmans CR et al

ALA and LA can act as sources for second messengers within and between neurons.Lock CA et al

DHA; It is estimated that only 5–15% of ALA is ultimately converted to DHA Holub,
influenced by age, disease, stress and omega-6 intake.Bourre JM
Synaptic membranes in the brain contain high levels of DHA, critical for transmission and membrane fluidity Heron DS et al
"epidemiological studies have reported the benefit of DHA in the prevention of age-related macular degeneration" Bretillon L et al
"Numerous epidemiological studies have highlighted the beneficial influence of DHA on the preservation of synaptic function in aged individuals. Oster T el al
DHA is related to brain health throughout the lifespan Muldoon MF et al Free Full Text

DPA and DHA have differential effects on visual signal transduction.Mitchell DC et al
DPA down-regulates the expression of genes involved in fat synthesis in liver cells. (not due to conversion) Kaur G et al
DPA appears principally derived from endogenous elongation from EPA, and DPA can also undergo retroconversion back to EPA.Mozaffarian D et al
DPA is specifically effective in inhibition of aggregation in platelets, in wound-healing processesKaur G et al

EPA acts as a precursor for prostaglandin-3 (which inhibits platelet aggregation), thromboxane-3, and leukotriene-5 groups.
EPA is a well documented inhibitor of proinflammatory cytokines such as IL-1 β and TNFα.

LA is used in the biosynthesis of arachidonic acid (AA) and eicosanoids.
It is also found in the lipids of cell membranes.
LA is partly converted into 9-hydroxyoctadecanoic acid and 13-hydroxyoctadecanoic acid, which activate TRPV1, the capsaicin receptor
, and through this might play a major role in hyperalgesia and allodynia.Patwardhan AM et al
LA is also partly converted into gamma-linolenic acid (GLA).
GLA is partly converted to dihomo-gamma-linolenic acid (DGLA),
which in turn is converted to arachidonic acid (AA).
AA is partly converted into eicosanoids: prostaglandins, thromboxanes and leukotrienes.

The effects of arachidonic acid (AA), EPA, and DHA supplementation on membrane incorporation, phospholipase A(2) catalyzed release and eicosanoid production.Norris PC et al
omega-3.jpg
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Lipid peroxidation

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Lipid peroxidation

All fatty acids are eventually subject to oxidation, but the route differs:
- particularly non-PUFAs are utilized for energy (aerobic meatbolism rendering reactive oxygen species (ROS)), eventually entering the Krebs cycle, in which they may be converted into Pyruvic acid (an alpha-keto acid) or alpha-Ketoglutaric acids which are potent Maillard precursors/intermediates (yielding CML etc).
- particularly PUFAs are vulnerable to lipid peroxidation (a radical chain reaction rendering lipid peroxyl radicals and lipid hydroperoxide), also yielding Maillard intermediates (and subsequently CML etc). As PUFAs are used for other purposes than energy (eicosanoids etc, see post above), PUFAs are protected against lipid peroxidation by antioxidants and enzymes.

Lipid peroxidation is catalyzed by all transition metals.
PUFAs are more volnerable to oxidation than monounsaturated fatty acids (eg palmitoleic acid Matthan NR) because they contain more than one double-bonded carbon units.
These multiple double-bonded carbon untits are separated by single bonded carbon units.
Such intermediate carbon units have the lowest C–H bond-energies (the least strong),
which makes them more volnerable to attack by ROS produced by aerobic metabolism, and peroxyls produced by lipid peroxidation.
Even if a pure lipid hydroperoxide is subjected to decomposition a great variety of products is generated,
since primary products suffer further transformations. (into 2-butenal, hexanal, 5-oxodecanal, buten-1,4-dial, 4-hydroxy-2-nonenal)Spiteller P et al.


The Maillard reaction and lipid peroxidation are intimately related

http://www.waiwiki.org/index.php/Maillard_reaction
Sugars, protein and fats are all sources of carbonyls, reactive Maillard intermediates that form AGEs and ALEs; markers for aging and disease.
Glucose and PUFAs may autoxidize to form reactive carbonyls, which may also be formed by the decomposition of Amadori compounds (amino acids plus sugars), oxidized protein, or lipid peroxidation.
Carbonyls readily react with amino groups in peptides, protein, nucleotides and phospholipids to form AGEs/ALEs.
Specific carbonyls may be lipid derived (eg acrolein, malondialdehyde), sugar derived (deoxyiosones, butanediones), or both (glyoxal, methylglyoxal).
Glyoxals are both aldehydes and ketones, and may yield CML, for example, in tissues a marker for aging.
Hyperglycemia, elevated intakes of PUFAs and elevated levels of amines all separately induce formation of AGEs/ALEs such as CML.

The so called base level of oxidative modification of lipids could be important to cell signaling, and membrane remodeling.
A high level of accumulation of lipid peroxidation accelerates the progress of aging Radak Z et al
The strength of our defense against excessive lipid peroxidation and AGEs/ALEs plays a key role.
Dietary cooked food-PUFAs may add to the influence of endogenous lipidoxidation, as they are decomposed by heat, generating LOOHs,
LO* and LOO* radicals. (generated by frying of fats) Spiteller G et al
These products are adsorbed in the intestine, and at least partly incorporated in low density lipoproteins (LDLs).
An overload of PUFAs induces only after two days an increase in oxidized LDL/PUFAs.Spiteller G

Formation of AGEs/ALEs is inhibited and counteracted by various enzymes, including fructosyl amine oxidases, aldolase B inhibitors and glutathione-dependent enzymes. Various antioxidants inhibit lipid peroxidation and AGE/ALE formation,
also inhibited or counteracted by vitamin B1, B3, B6, pyridoxamine, alpha-lipoic acid, taurine, oleic acid, oleanolic acid and ursolic acid.
ALA is more susceptible to lipid peroxidation, but ALA also suppresses oxidative stress.Yilmaz O et al
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Oxygen sensitivity of PUFAs

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Of course, the big question is:
Why does nature use PUFAs for essential processes, as they are relatively susceptible to oxidation?
Answer: because they are oxygen-sensitive!

"nature uses this sensitivity for signalling processes by producing lipidhydroperoxides (LOOHs) by any change to cell membrane structure."
So, its the sensitivity of PUFAs that will notice damage.
And its degradation products serve as signalling compounds, to induce actions.
"LOOHs produced in enzymic reactions are degraded specifically to signal compounds which induce physiological responses" Spiteller G, through activation of genes.
"cancer might be the consequence of a low response of cells to induce apoptotic (cell death/suicide) lipid peroxidation processes".Spiteller G

So, the susceptibility of PUFAs to oxidation is part of our defense against cancer,
and other 'attacks' that compromise the original functioning of cells.
The susceptibility of PUFAs to oxidation induces cell death before cells can go astray.
Oxidation products of PUFAs may serve various other signalling functions;
"several oxidation products of linoleic acid (LA) affect production of aldosterone and corticosterone" Goodfriend TL et al
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Enzymatic / non-enzymatic lipidoxidation

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Enzymatic lipoxidation
Reactive oxygen species (ROS) create damage. The protein that become damaged by ROS are often located in specific regions of the cell membrane.
The damage/changes to those proteins mediate redox-sensitive processes such as autophagy, the antioxidant response, and apoptosis. Cummins, TD et al
Whenever the membrane gets damaged / altered, due to cell proliferation, wounding (by ROS) or aging,
and also by the extend of synaptic activity, phospholipases in the membrane are activated.
Also metals such as copper may induce redux cycling, evoking lysosomal membrane damage by ROS, causing the release of cytotoxic digestive enzymes.Pourahmad J et al
These phospholipases cleave specific phospholipids localized in the phospholipid layer of the cell wal (membrane reservoirs), which liberates PUFAs.
These PUFAs are broken down by lipoxygenases (LOX), which generates lipid hydroperoxides (LOOHs).Bazan NG et al Bazan
Many oxidized lipid products are electrophilic; the RLS (reactive lipid species).
Cell signalling by electrophiles appears to be limited to the modification of cysteine residues in proteins.Higdon A et al
Cysteine evokes the reduction of ferric to ferrous iron, initiating peroxidation, subsequently (after 1 hour) creating protein carbonyls. Yin D et al
Glutathione and associated enzymes insulate the signalling domain from uncontrolled electrophilic stress.
The damaged proteins are removed by the lysosome-autophagy pathway Higdon A et al Full Free Article
Bivalent metal ions within the active site of LOX catalyse this LOOH production.
LOOHs produce lipid messengers, which modulate signaling cascades, contributing to development, differentiation, function (e.g., memory)
, protection, regeneration, and repair of neurons and overall regulation of neuronal, glial, and endothelial cell functional integrity. Bazan NG et al Bazan
The metal ions generate radicals which are transformed within the enzyme complex to non-radical molecules.
"peroxyl radicals generated as intermediates cannot leave the enzyme complex" Spiteller G
"Thus radicals never leave the enzyme complex except in severe stress situations." Spiteller G

Non-enzymatic lipoxidation
If the amount of free PUFAs (the impact of the damage/change/attack) exceeds a certain amount, LOX commit suicide. (in severe stress situations)Spiteller G
Thats where the enzymatic reaction switches to a non-enzymic reaction.
This suicide liberates free iron ions that react with LOOHs (nonenzymic lipid peroxidation), creating radicals.Spiteller G
These peroxylradicals (LOO*) are not liberated enzymically, and thus they are not trapped within the enzym complex.
Peroxylradicals generate a second set of signalling compounds, but also cause severe damage.Spiteller G
LOOHs produced in nonenzymic reaction induce generation of ROS (reactive oxygen species) and cell death (apoptosis).
Non-enzymatic lipoxidation and elevated apoptosis are involved in all inflammatory diseases
and associated with the oxidation of a great variety of biological compounds, including proteins and nucleic acids.
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

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The cell suicide is a good thing, given the cell mutates into a cancer cell, in itself, but this results in ALOT of bad reactions.
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

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overkees wrote:the cell suicide is a good thing in itself, but this results in ALOT of bad reactions.
Actually, these radicals only get released due to extreme stress, resulting in non-enzymatic lipoxidation.
In enzymatic lipoxidation, these radicals remain within the enzyme system, and are neutralised.

In enzymatic lipoxidation, one of the messengers created from DHA, is neuroprotectin D1; NPD1 (10,17S-docosatriene).
When retinal pigment epithelial cells are exposed to,oxidative stress, NPD1 is synthesized.
"NPD1 potently counteracts oxidative stress-triggered apoptotic DNA damage in RPE,
upregulates antiapoptotic proteins Bcl-2 and Bcl-x(L), and decreases proapoptotic Bax and Bad expression".Bazan NG et al
NPD1 protects against cell damage from from oxidative-stress Mukherjee PK et al mediated by aging/disease. Mukherjee PK et al
"Deficits in DHA or its peroxidation (NPD1) appear to contribute to inflammatory signaling, cell death,
and neuronal dysfunction in Alzheimer disease (AD)". (age-related neurological disorder) Lukiw WJ et al
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Optimal PUFA intake

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PUFA lipoxidation increases with age, and disease,
which is logical, as associated with a decreased antioxidative and enzymatic defense.

Scientific literature has also shown us that there multiple reasons why PUFAs are incorporated in membranes.
Literature has also shown that there is a logical reason why PUFAs are sensitive to lipoxidation,
and also that there is a biological function for lipoxidation.
Excessive lipoxidation is harmful, there is no doubt about that.
Its interesting that cooked foods burden the body with both intermediates and advancced lipoxidation end-products.
And that cooked foods also burden the body with glycation products that may induce endogenous lipoxidation.

PUFAs are essential, and epidemiological studies show that their availability is positively linked to longevity.
Excessive PUFAs may however induce endogenous lipoxidation (which is inhibited by the body's antioxidative defense, including enzymes)
, so that we yet need to establish the optimal intake of PUFAs.
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Copper-triggered CML formation

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CML can be formed through glycation, fructation or lipid peroxidation. So, let’s look at the CML concentrations that get formed by administration of either Arachidonate, Linoleate or Oleate and Glucose[1]:
CMLcomparison.jpg
Polyunsaturated fats also quite easily form other AGEs, such as malondialdehydelysine (MDA-lys) and carboxyethyllysine (CEL).
MDA-lys in brain was increased by more than 150% and MDA-lys in liver by more than 50%.
proproteinmodificationmarkers.gif
The composition of the SAT diet was identical to that of the UNSAT diet except that 9.5% hydrogenated coconut oil plus 0.5% corn oil were present as fat source instead of 10% menhaden oil. The amount of food ingested did not show significant differences between groups.
"These results, together with previous data from our laboratories, show that increasing the degree of fatty unsaturation of postmitotic tissues in vivo can raise not only lipid but also protein and mtDNA oxidative damage." [2]

Some notifications:
Menhaden oil is high in omega 3s. 30% PUFAs, of which 29% are omega 3
So, of the 10%, 30% are PUFAs. This means that 3% out of the complete diet was omega 3 was the only difference in diets.
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Copper-triggered CML formation

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Yes, the Maillard reaction and lipid peroxidation are closely intertwined.
CEL, CML and malonaldehyde are just a few of their intermediates / end-products.
All fatty acids, but also all proteins and carbs readily provide the carbonyls involved in forming such ALEs/AGEs.
And not just lipid peroxidation, but all radical reactions are chain reactions.
Oleic acid (oleate) is a known (relative) inhibitor of lipid peroxidation.
For more info about all this:
http://www.waiwiki.org/index.php/Maillard_reaction
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Re: Copper-triggered CML formation

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Understand the implications: only 3% of extra omega3s in the diet in rats had such a huge effect on malondialdehydelysine (MDA-lys) formation. "MDA-lys in brain was increased by more than 150% and MDA-lys in liver by more than 50%." And what a burden it has on protein modifcation markers.
Also look how AA is so much more CML producing than LA.
These results all indicate to me that you really don't want too much PUFAs and that 3% was already enough to aggrevate alot of things.
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

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In your first article, about CML, the antioxidants were removed and copper was added.
In your second article, besides the marked increase in MDA-lysine,
in the liver CML and CEL were significantly lower (20–29%) in the UNSAT than in the SAT group.
overkees wrote:Understand the implications: only 3% of extra omega3s in the diet in rats had such a huge effect on malondialdehydelysine (MDA-lys) formation. "MDA-lys in brain was increased by more than 150% and MDA-lys in liver by more than 50%
Only 3% extra omega-3s?
Total fat in SAT diet: 95% hydrogenated coconut oil (1.65% PUFA) plus 5% corn oil (1% PUFA) = 1.6% PUFA
Total fat in UNSAT diet: 100% menhaden oil = 30% PUFA

So, the UNSAT diet contained 18-fold more PUFA (1775%) than the SAT diet. (not just 3% extra PUFA).
Quite extreme, dont you think?
Particularly when compared to the much smaller increase in MDA-lys (150%)
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Poly-unsaturated fatty acids

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The diet was:
The composition of the UNSAT diet was: cornstarch 36.75%, purified casein high nitrogen 20%, dextrinized corn starch 13.2%, sucrose 10%, menhaden oil 10%, alphacel non-nutritive bulk 5%, AIN-93G mineral mix 3.5%, AIN-93 vitamin mix 1%, l-cystine 0.3%, choline bitartrate 0.25% and t-butyl hydroquinone 0.0014%. The composition of the SAT diet was identical to that of the UNSAT diet except that 9.5% hydrogenated coconut oil plus 0.5% corn oil were present as fat source instead of 10% menhaden oil.
The total caloric intake in the UNSAT diet is 3% omega 3s.
I don't think it's quite extreme, as the setup of the research is to show a difference between unsaturation to saturation. And as you can see, on a diet that contained almost no PUFAs (the SAT diet) has a lot less damage.

On exactly the same diets another research was done to investigate other issues:
“Lipid peroxidation of heart mitochondria was significantly different between the two groups, the values in the UNSAT group reaching 255% of those in the SAT group (Fig. 3). Three different markers of protein oxidative damage also showed significant differences as a function of the degree of unsaturation of mitochondrial fatty acids. MDA-lys was the protein marker more profoundly affected since its levels in the UNSAT group were 186% of those present in the SAT group (Fig. 3). Protein carbonyls were also stimulated by fatty acid unsaturation, UNSAT levels reaching 153% of those present in the SAT group (Fig. 3). CML was the protein modification marker less profoundly affected. Even so, CML values were again significantly higher in UNSAT than in SAT mitochondria (Fig. 3).”

RRM, it is really necessary to get insight in what levels of PUFAs are really essential. There are alot of researches that point to dangers of relatively small amounts of dietary PUFAs, it is therefore necessary to establish a safe upper limit.
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

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So, a diet 1775% higher in PUFA (3-fold higher than recommended; 30% of total fat intake)
caused a maximal increase in lipid peroxidation products of 150%
(or even a decrease, for some products in the liver)
Thats not at all spectacular...
on a diet that contained almost no PUFAs (the SAT diet) has a lot less damage
Actually, im surprised that even on a diet with 1775% less PUFA, there is only 150% less (MDA-lys) damage.
Meaning that a drastic reduction in PUFAs has relatively small effects on lipoxidation product levels.
So that even if you minimize PUFA intake, lipid peroxidation markers are significant.
overkees wrote:RRM, it is really necessary to get insight in what levels of PUFAs are really essential.
Of course, I agree.
But also what levels are beneficial.
Lipid peroxidation is just one aspect of health, lets not forget that.
Regarding many aspects of health, higher intakes of omega-3 are very beneficial.
There are alot of researches that point to dangers of relatively small amounts of dietary PUFAs
Which ones?
Its very interesting to see that a huge (1775%) reduction in PUFA (resulting in only 0.2% PUFA of total energy),
translates to (only) 150% less MDA-lys and other lipoxidation products.
Thats how little effect minimizing PUFA has (in that study).
Does a diet containing 0% PUFA actually result in drastic lower lipoxidation products?
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Preventing lipid peroxidation

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101 free-living individuals eating their habitual diets had fish consumptions ranging from less than one serving per week to over five servings per week,
correlating with serum EPA (20:5), DHA (22:6), and total n-3 PUFA, and in the phospholipid and cholesterol ester fractions of isolated LDL.
When isolated LDL were subjected to Cu2+-induced ex vivo oxidation,
higher n-3 PUFA (22:6 and 20:5) correlated with lower oxidation parameters.
In contrast, intake of n-6 PUFA (20:4 and 18:2) positively correlated with the two oxidation parameters.de Ruiz GJ et al

Instead of minimizing PUFA (with relatively small preventative effects), an optimal antioxidant defense may be key:

Olive oil has been shown to contain antioxidants effectively inhibiting lipid peroxidation.Casal S et al
When lambs were fed 10% linseed oil (=68% PUFA) + 17% olive cake, which increases PUFA in phospholipids,
and vitamin E in muscle, without compromising its oxidative stability (fatty acid peroxides, oxidized cholesterol),
in contrast to the lambs fed the 10% linseed but not the olive cake. Luciano G et al

Its actually the intake of omega-3 (and the resulting protein adducts) that stimulates the anti-lipoxidation defense.
There is a time-dependent effect of n-3 PUFAs on the antioxidant response systems in the heart.
Not after 3 weeks, but after 14 weeks, "expression and activity of key enzymes involved in antioxidant and phase II detoxification pathways ...
were elevated in hearts from mice fed the n-3 PUFA diet,
but not in hearts from mice fed the diet containing almost no PUFA. Anderson AJ et al

The influence of 6 weeks of long chain PUFA (600 mg EPA and 400 mg DHA per day) supplementation
+ 30 mg vitamin E + 60 mg vitamin C + 6 mg β-carotene
on resting and exercise-induced lipid peroxidation in judoists (n = 36).
... consumption of an n-3 LC PUFA supplement increased oxidative stress at rest and did not attenuate the exercise-induced oxidative stress.
The addition of antioxidants did not prevent the formation of oxidation products at rest.
In contrast, the combination of antioxidants added to the n-3 PUFA supplement led to a decrease in
malondialdehyde and lipoperoxide concentrations after a judo training session.Filaire E et al

Vitamin E plus plant polyphenols may reduce oxidation by 48% in cows supplemented with ALA (5% linseed oil) Gobert M et al
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Re: Poly-unsaturated fatty acids & Lipid peroxidation

Post by overkees »

Look, the 1775% might sound huge and impressive, but please not that there will still be PUFAs in the tissues of the animals. And that the animals also probably start producing mead acid. You've got to take that into consideration. That percentage itself doesn't say much, that's what I think.

We've also got to take into consideration that if you restrict PUFAs, there will be a release of old PUFAs into the blood. On a longer term I think the effect will be increased more and more. 7 weeks is not very long.

Have you read this post?

Do you also think all these differences are perfectly fine too when the antioxidant system is functioning properly? What are the huge benefits of relatively high levels of omega 3 you are constantly talking about? Can you give me some examples, then I can review them.
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