Mercaptoethanol and Aging

[Martin Ban]

If humans ingest ethanol, they are probably going to form some
mercaptoethanol. Only mercaptoethanol has been able to shift
the death curve to the right in rodents (increase both the
median and maximum life span).

Mech Ageing Dev 1984 Oct31;27(3):341-358.

"Can antioxidant supplementation slow the aging process?"
Biofactors 1998;7(1-2):93-101.

This is a review article that points out that of all of the
antioxidants tried, only mercaptoethanol works (0.25% added to
the feed). The first paper cited is one of these studies.

In rats, mercaptoethanol (13 micrograms per 100 grams body
weight) coming in every day in the feed for two weeks
decreases protein synthesis in 2-year old rats (rats loose
less protein and form less urea). J Comp Physiol [B]
1992;162(6):547-551. Yes, I know that the smell may have
resulted in less food intake but the investigators apparently
took this into account. If I understand rats correctly kidney
failure is usually what gets them and this study showed that
mercaptoethanol would lower the solute load on the kidneys in
very old rats.

In old mice, mercaptoethanol prevented the loss of nerve
terminals in the small intestine that occur with aging. Dose
is not indicated but the mice where given water with
mercaptoethanol in it for 17 months and then nerve terminal
density in the small intestine was examined. Exp Gerontol
1990;25(2):135-140.

Mercaptoethanol preserves brain function in old mice. 8
micrograms per animal per day in water was given at 5 months
and then continuous until 24 months. Dopamine release declines
with age. Not only did dopamine not decline with age in the
treated mice, it was higher than normal compared to what is
seen at 5 months of age. Pharmacology 1990;40(6):343-348.

Mercaptoethanol protects mice from cigarette smoke. Putting
mice in a smoke filled room caused spontaneous death of some
of the mice. In addition, the incidence of hepatocellular
carcinoma increased. Giving these animals mercaptoethanol
prevented the detrimental effect of breathing the smoke every
day. Immune function was depressed by the smoke and
mercaptoethanol brought reactivity against sheep erythrocytes
up to a level that was higher than the control (mice with no
smoke exposure). Gerontology 1991;37(6):326-334.

The human immune system declines with age. Mercaptoethanol
prevents this decline in mice. One study actually looked to
see if mercaptoethanol could help human T lymphocytes just
like it does for old mice. Old healthy humans had blood drawn
and the T lymphocytes were challenged with TPA, A T-cell
mitogen. A mitogen makes T cells divide. Old human T cells do
not divide very well. Putting mercaptoethanol in the culture
media made the old cells act just like young human T-cells do.
Geronotology 1985;31(1):39-45.

"Effect of 2-mercaptoethanol on some metabolic indices of
ageing of CBA/Ca inbred mice" Mech Ageing Dev 1988
Oct;45(1):75-92. First line of this abstract:

"It has been shown in several studies that 2-mercaptoethanol
(2-ME) improves the life span and aspects of life performance
of laboratory animals." I did not go back any further than
1988. I cited only about 1/2 of the abstracts that I printed
out and I did not print out all of the studies where
mercaptoethanol was used. It appears that mercaptoethanol
works as well or maybe even better than calorie restriction
for life extension.

It also appears that humans will form mercaptoethanol
everytime that ethanol comes into the human body. The
interesting thing about this possibility is that people with
a very high liver alcohol dehydrogenase activity probably
will not get as much mercaptoethanol as the ones with a much
lower liver alcohol dehydrogenase activity. The ones with
the low activity are often referred to as "cheap drunks".
They get drunk on very little ethanol. The other factor that
will probably determine how much mercaptoethanol is formed
is the sulfate status of the liver and other tissues in the
human body.

Tom and his buddies in sci.life-extension are wasting their
time and their money popping antioxidant supplements. Even
lipoic acid does not work in
mice. Mice have a much poorer antioxidant defense system than
we do, if it can't work in mice it certainly is not
going to work in us.

While looking for this mercaptoethanol data I found some very
good data on antioxidant levels and antioxidant enzyme
activities in humans as we age. I'll start a new thread with
this human data and why vitamin C is no good for humans (it's
role has been taken over by uric acid and if you take more
than what is needed for collagen synthesis you increase free
radical damage rather than decrease it). If you like to
believe the bible, God told us not to eat food with vitamin C
in it (don't eat the apple).

--
Marty B. "You are what you eat."

http://centernet.okstate.edu/nutrition/index.html

The above website is for educational purposes only. Material
in this website and posted material represents the opinion of
Martin Banschbach, Ph.D. and does not reflect Oklahoma State
University policy or position on nutrition.

Issues regarding the diagnosis and treatment of human disease
can not be addressed by material in the above website or by
Martin Banschbach, Ph.D.

Any comments made by Martin Banschbach, Ph.D. are invalid
unless confirmed by your personal physician.

[Steve Harr]

Martin Banschbach PhD wrote in message ...

> If you like to believe the bible, God told us not
> to eat food with vitamin C in it (don't eat the apple).

Well, the bible says nothing about apples. Just the fruit of
two particular trees. I think Adam and Eve should have done it
in reverse order, but then it wouldn't have been so good a
story, would it? As it is we living here in the East of Eden
have the worst of both worlds, we're going to die, and we KNOW
we're going to die. That puts us halfway between animals and
gods; and that's the metaphor.

SBH

--
I welcome email from any being clever enough to fix my
address. It's open book. A prize to the first spambot that
passes my Turing test.

[Alf Christ]

On Tue, 26 Feb 2002 13:32:13 -0600, "Martin Banschbach PhD"
<mbansch@osu-com.okstate.edu> wrote:

>If humans ingest ethanol, they are probably going to form
>some mercaptoethanol. Only mercaptoethanol has been able to
>shift the death curve to the right in rodents (increase both
>the median and maximum life span).

If you look for mercaptoethanolamine, you will find that it
is formed from cysteine and not from alcohol. And
mercaptoethanolamine is a source for hypotaurine, a wellknown
antioxidant (which is rather quickly transformed into
taurine) Was any of these compounds ever tested in the same
system?? I doubt it.

[Db]

Martin Banschbach PhD wrote:

<snip>

> It also appears that humans will form mercaptoethanol
> everytime that ethanol comes into the human body. The
> interesting thing about this possibility is that people with
> a very high liver alcohol dehydrogenase activity probably
> will not get as much mercaptoethanol as the ones with a much
> lower liver alcohol dehydrogenase activity. The ones with
> the low activity are often referred to as "cheap drunks".
> They get drunk on very little ethanol. The other factor that
> will probably determine how much mercaptoethanol is formed
> is the sulfate status of the liver and other tissues in the
> human body.

But those people with lower dehydrogenase activity will also
have reduced toxicity from the alcohol due to the quicker
conversion of acetaldehyde into acetic acid, correct? And the
fact that they do not need to drink as much to get drunk.

> Tom and his buddies in sci.life-extension are wasting their
> time and their money popping antioxidant supplements. Even
> lipoic acid does not work in
> mice. Mice have a much poorer antioxidant defense system
> than we do, if it can't work in mice it certainly is
> not going to work in us.

Those antioxidants will affect *average* lifespan of
course by reducing the development of disease. I have a
hard time believing that the antioxidant activity of
mercaptoethanol could extend maximum lifespan. It must do
something else as well.

>
> While looking for this mercaptoethanol data I found some
> very good data on antioxidant levels and antioxidant enzyme
> activities in humans as we age. I'll start a new thread with
> this human data and why vitamin C is no good for humans
> (it's role has been taken over by uric acid and if you take
> more than what is needed for collagen synthesis you increase
> free radical damage rather than decrease it). If you like to
> believe the bible, God told us not to eat food with vitamin
> C in it (don't eat the apple).

But you can't just take C alone. It needs to be regenerated by
other antioxidants.

[Db]

DB wrote:

> But those people with lower dehydrogenase activity will
> also have reduced toxicity from the alcohol due to the
> quicker conversion of acetaldehyde into acetic acid,
> correct? And the fact that they do not need to drink as
> much to get drunk.

Whoops. I meant higher activity.

[Martin Ban]

alf.christophersen@basalmed.uio.no (Alf Christophersen) wrote
in message news:<3c7c0e1b.14227555@nntp.uio.no>...

> If you look for mercaptoethanolamine, you will find that it
> is formed from cysteine and not from alcohol. And
> mercaptoethanolamine is a source for hypotaurine, a
> wellknown antioxidant (which is rather quickly transformed
> into taurine) Was any of these compounds ever tested in the
> same system?? I doubt it.

Why not look Alf? You can do a medline search as well as I
can. Mercaptoethanolamine is only going to give you 3 hits.
With Mercaptoethylamine, you will probably get as many hits as
I got for mercaptoethanol and ageing.

If I remember correctly mercaptoethylamine is also called
cysteamine. I would image that both hypotaurine and
mercaptoethylamine have been looked at in mice. These are both
going to come from cysteine metabolism. I got off on this
tangent when wine was being discussed. Could ethanol without
any bioflavinoids still have a positive effect in humans?

Why don't you work up mercaptoethylamine and hypotaurine?

[Martin Ban]

DB <wired123@pacbell.net> wrote in message news:<ceUe8.6820$V-
R6.3396162767@newssvr21.news.prodigy.com>...

> But you can't just take C alone. It needs to be regenerated
> by other antioxidants.

No, C can regenerate itself. Two C free radicals will react
together to form 1 molecule of reduced C and 1 molecule of
oxidized C (dehydroascorbate).

[Alf Christ]

On 26 Feb 2002 18:11:38 -0800, mbansch314@aol.com (Martin
Banschbach) wrote:

>Why don't you work up mercaptoethylamine and hypotaurine?

It was a typo. Cysteamine is the reduced version of
hypotaurine. That is, RSH, where hypotaurine is RSO2H and
taurine is RSO3H where R is the same structure. From
homocysteine you may get homotaurine (and most possibly
mercaptopropylamine and hypohomotaurine (both of which I have
never seen in literature). In some aspects, the homocysteine
derivatives has different effects than the cysteine
derivatives. Cysteine-> cysteamine pathway is possibly not the
dominant mainway unto taurine, but rather the dioxygenase ->
decarboxylation pathway where the dioxygenase is published to
be the rate limiting step.