Re: Vitamin E in the autoimmune mechanism

On 28 Dec 2006 12:16:40 -0800, monty1945@xxxxxxxxx wrote:

Tom:

Did you happen to notice that they suggested lipid peroxidation as
underlying cause? Are you aware that a saturated fatty acid is not
subject to this?

Ah...not true (the second statement). Saturated fatty acids can become
rancid. Susceptibility for lipid peroxidation is higher for mono- and
polyunsaturated fatty acids, however, it happens for saturated fatty
acids. Depends in part on the chain length.

Yes, Vitamin E is one of the major antioxidants that prevent free
radical damage associated with lipid peroxidation.

Interesting study shows the use of alcohol and fish oil is harder on
the liver than when taken with medium chain triglycerides. That's in
rats so caution when applying to humans (or Finns or Swedes...):
http://jpet.aspetjournals.org/cgi/content/abstract/299/2/638

Note further the difference between saturated fats and trans fats,
e.g., http://atvb.ahajournals.org/cgi/reprint/21/7/1233.pdf

Your simplistic notions are divorced from reality, monty. Let alone
inchoate, irrelevant and perverse.

George M. Carter

**
Balasubramanian KA, Nalini S, Cheeseman KH, Slater TF. Nonesterified
fatty acids inhibit iron-dependent lipid peroxidation. Biochim Biophys
Acta. 1989 Jun 28;1003(3):232-7.

Christian Medical College Hospital, Vellore, India.

The effect of various fatty acids on lipid peroxidation of liver
microsomes induced by different methods in vitro was studied using
oxygen uptake and malonaldehyde (MDA) production. It was observed that
fatty acids with a single double bond are effective inhibitors of
peroxidation. Stereo and positional isomers of oleic acid were equally
effective as oleic acid. There was an absolute requirement for a free
carboxyl group, since methyl esters of fatty acids and long-chain
saturated and unsaturated hydrocarbons could not inhibit peroxidation.
Saturated fatty acids with a chain length of 12-16 carbon atoms showed
inhibition, whereas more than 18 carbon atoms reduced the inhibitory
capacity. Fatty acids of lower chain length such as capric and
caprylic acids did not show inhibition. Fatty acid inhibition was
partially reversed by increasing the concentration of iron in the
system. Peroxidation induced by methods which were independent of iron
was not inhibited by fatty acids. It was observed that intestinal
microsomes which were resistant to peroxidation due to the presence of
nonesterified fatty acids in their membrane lipids were able to
peroxidise by methods which do not require iron. These results suggest
that certain fatty acids inhibit peroxidation by chelating available
free iron. In addition, they may also be involved in competing with
the esterified fatty acids in the membrane lipids which are the
substrates for peroxidation.

***
By contrast, maybe not so good for the rats' nuts...

E Rosenblum, JS Gavaler and DH Van Thiel. Lipid peroxidation: a
mechanism for ethanol-associated testicular injury in rats
Endocrinology, Vol 116, 311-318,

Chronic alcohol administration leads to hepatic membrane alterations
which, at least in part, are due to lipid peroxidation and may
contribute to the toxicity of ethanol at the level of the hepatocyte.
Because changes in testicular function also occur after chronic
administration of ethanol to rats, we evaluated testicular
mitochondria for evidence of alcohol-associated peroxidation injury
which might contribute to the gonadal injury that occurs with
prolonged use of the drug. Lipid peroxidation was assessed through
measurement of diene conjugates, polyenoic fatty acid composition,
malonaldehyde formation, and testicular reduced glutathione levels.
Compared to isocalorically matched dextrimaltose-fed controls (ISO),
rats fed alcohol (ETOH) for 50 days had a decreased content of
polyenoic acids and a compensatory increase in saturated fatty acids
[ETOH, 50.69 +/- 0.65% (by wt); ISO, 52.93 +/- 0.72 (mean +/- SE); P
less than 0.01]. This decrease in polyunsaturated fatty acid content
was accompanied by an increase in diene conjugates in testicular
mitochondria (ETOH, 0.455 +/- 0.053 OD units at 233 nm/mg lipid; ISO,
0.382 +/- 0.045; P less than 0.05). An increase in malonaldehyde
formation also was observed in the alcohol- fed rats compared to the
control level (ETOH, 21.39 +/- 1.67 nmol/mg protein; ISO, 17.50 +/-
1.39; P less than 0.05) as well as a decrease in glutathione content
(ETOH, 1218 +/- 89 micrograms GSH/testes; ISO, 1638 +/- 89; P less
than 0.05). Taken together, these findings support the concept that
lipid peroxidation may be an important mechanism responsible, at least
in part, for the toxic effect of ethanol on the testes.

.

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