On Jul 27, 2:00 pm, ken <flakey...@earthlink.net> wrote: snip <<

Dance .. atheist ..

"Maltol restored glutathione"

Glutathione—a review on its role and significance
in Parkinson’s disease
Published online before print June 19, 2009
Heather L. Martin and Peter Teismann
E-mail contact: p.teism...@abdn.ac.uk

Parkinson’s disease (PD) is the second most common
neurodegenerative disease, affecting over a million
people in the United States alone, and is characterized
by rigidity, bradykinesia, resting tremor, and postural
instability.
Its main neuropathological feature is the loss of
dopaminergic neurons of the substantia nigra pars compacta.
However, the pathogenesis of this loss is not understood
fully.
One of the earliest biochemical changes seen in PD is a
reduction in the levels of total glutathione, a key cellular
antioxidant.
Traditionally, it has been thought that this decrease in
GSH levels is the consequence of increased oxidative stress,
a process heavily implicated in PD pathogenesis.
However, emerging evidence suggests that GSH depletion may
itself play an active role in PD pathogenesis.
This review aims to explore the contribution of GSH depletion
to PD pathogenesis.
—Martin, H. L., Teismann, P. Glutathione—a review on its role
and significance in Parkinson’s disease.

-----------------

"Maltol remarkably attenuated the neurobehavioral signs and neuronal
loss"

"Leading to a decrease in mortality of animals to 12.5%"

Neuroprotective Effect of Maltol Against Oxidative Stress in Brain of
Mice Challenged with Kainic Acid
Authors: Yun-Bae Kim a;  Sang Hee Oh b;  Dai-Eun Sok; Mee Ree Kim b
Affiliations:    a College of Veterinary Medicine and Research
Institute of Veterinary Medicine, Chungbuk National University,
Cheongju, South Korea
b Department of Food and Nutrition and Cancer Research Institute,
College of Pharmacy, Chungnam National University, Taejon, South
Korea

Abstract
The neuroprotective effect of maltol on oxidative damage in the brain
of mice challenged with kainic acid was examined.
Male ICR mice, 6-8 weeks of age, were administered orally with maltol
(50 or 100 mg/kg) for 5 consecutive days.
Thirty minutes after the final administration, the animals were
challenged s.c. with kainic acid (50 mg/kg), and neurobehavioral
activities were monitored.
In addition, biomarkers of oxidative stress and neuronal loss in
hippocampus for the biochemical and morphological evaluations were
analyzed 2 days after the kainic acid challenge.
During 5-day treatment with maltol, the body weight gain was not
significantly different from that of vehicle-treated control animals.
Administration of kainic acid alone induced severe epileptiform
seizures, causing a lethality of approximately 50%, and injuries of
pyramidals cells in hippocampus of mice survived the challenge.
Kainic acid exposure also resulted in marked decreases in total
glutathione level and glutathione peroxidase activity, and an
increase
in thiobarbituric acid-reactive substances (TBARS) value in brain
tissues.
In comparison, coadministration with maltol (100 mg/kg) remarkably
attenuated the neurobehavioral signs and neuronal loss in
hippocampus,
leading to a decrease in mortality of animals to 12.5% (p<0.05),
although maltol at a dose of 50 mg/kg failed to show any remarkable
protection.
In addition, the changes in glutathione and TBARS values and
glutathione peroxidase activity induced by kainic acid were restored
to control levels by pretreatment with maltol (100 mg/kg).
On the basis of these results, maltol is suggested to be a functional
agent to prevent the oxidative damage in the brain of mice.

Keywords: Glutathione; Kainic acid; Lipid peroxidation; Maltol;
Neuroprotection; Maltol, butanol fraction from methanol extract of
Thunb; GSH, reduced glutathione; KA, kainic acid; DTNB, 5,5'-
dithiobis
(2-nitrobenzoic acid); TBARS, thiobarbituric acid-reactive
substances

---------

"Maltol"

Comparative study of iron mobilization from haemosiderin, ferritin
and
iron(III) precipitates by chelators.
Kontoghiorghes GJ, Chambers S, Hoffbrand AV.
The heteroaromatic chelators 1,2-dimethyl-3-hydroxypyrid-4-one,
maltol, mimosine and 2,4-dihydroxypyridine-N-oxide, have been shown
to
mobilize iron from human spleen haemosiderin, ferritin and also from
iron(III) precipitates, all containing equal amounts of iron, at
physiological pH.
In the case of almost every chelator, the least-solubilized
polynuclear iron form was ferritin, whereas haemosiderin was more
soluble and the iron(III) precipitate the most soluble of all.
Most of the chelators were more efficient than desferrioxamine at
releasing iron from ferritin, but less efficient in the removal of
iron from the other two polynuclear iron forms.
It is suggested that the chelator differences in iron mobilization
may
be related to variations in the chelator molecular structure, the
protein structure, iron forms and in the mechanism of iron release.

PMID: 3566714

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/634q5a

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

Spamming Fuckhead

"Maltol restored glutathione"

Glutathione—a review on its role and significance
in Parkinson’s disease
Published online before print June 19, 2009
Heather L. Martin and Peter Teismann
E-mail contact: p.teism...@abdn.ac.uk

Parkinson’s disease (PD) is the second most common
neurodegenerative disease, affecting over a million
people in the United States alone, and is characterized
by rigidity, bradykinesia, resting tremor, and postural
instability.
Its main neuropathological feature is the loss of
dopaminergic neurons of the substantia nigra pars compacta.
However, the pathogenesis of this loss is not understood
fully.
One of the earliest biochemical changes seen in PD is a
reduction in the levels of total glutathione, a key cellular
antioxidant.
Traditionally, it has been thought that this decrease in
GSH levels is the consequence of increased oxidative stress,
a process heavily implicated in PD pathogenesis.
However, emerging evidence suggests that GSH depletion may
itself play an active role in PD pathogenesis.
This review aims to explore the contribution of GSH depletion
to PD pathogenesis.
—Martin, H. L., Teismann, P. Glutathione—a review on its role
and significance in Parkinson’s disease.

-----------------

"Maltol remarkably attenuated the neurobehavioral signs and neuronal
loss"

"Leading to a decrease in mortality of animals to 12.5%"

Neuroprotective Effect of Maltol Against Oxidative Stress in Brain of
Mice Challenged with Kainic Acid
Authors: Yun-Bae Kim a;  Sang Hee Oh b;  Dai-Eun Sok; Mee Ree Kim b
Affiliations:    a College of Veterinary Medicine and Research
Institute of Veterinary Medicine, Chungbuk National University,
Cheongju, South Korea
b Department of Food and Nutrition and Cancer Research Institute,
College of Pharmacy, Chungnam National University, Taejon, South
Korea

Abstract
The neuroprotective effect of maltol on oxidative damage in the brain
of mice challenged with kainic acid was examined.
Male ICR mice, 6-8 weeks of age, were administered orally with maltol
(50 or 100 mg/kg) for 5 consecutive days.
Thirty minutes after the final administration, the animals were
challenged s.c. with kainic acid (50 mg/kg), and neurobehavioral
activities were monitored.
In addition, biomarkers of oxidative stress and neuronal loss in
hippocampus for the biochemical and morphological evaluations were
analyzed 2 days after the kainic acid challenge.
During 5-day treatment with maltol, the body weight gain was not
significantly different from that of vehicle-treated control animals.
Administration of kainic acid alone induced severe epileptiform
seizures, causing a lethality of approximately 50%, and injuries of
pyramidals cells in hippocampus of mice survived the challenge.
Kainic acid exposure also resulted in marked decreases in total
glutathione level and glutathione peroxidase activity, and an
increase
in thiobarbituric acid-reactive substances (TBARS) value in brain
tissues.
In comparison, coadministration with maltol (100 mg/kg) remarkably
attenuated the neurobehavioral signs and neuronal loss in
hippocampus,
leading to a decrease in mortality of animals to 12.5% (p<0.05),
although maltol at a dose of 50 mg/kg failed to show any remarkable
protection.
In addition, the changes in glutathione and TBARS values and
glutathione peroxidase activity induced by kainic acid were restored
to control levels by pretreatment with maltol (100 mg/kg).
On the basis of these results, maltol is suggested to be a functional
agent to prevent the oxidative damage in the brain of mice.

Keywords: Glutathione; Kainic acid; Lipid peroxidation; Maltol;
Neuroprotection; Maltol, butanol fraction from methanol extract of
Thunb; GSH, reduced glutathione; KA, kainic acid; DTNB, 5,5'-
dithiobis
(2-nitrobenzoic acid); TBARS, thiobarbituric acid-reactive
substances

---------

"Maltol"

Comparative study of iron mobilization from haemosiderin, ferritin
and
iron(III) precipitates by chelators.
Kontoghiorghes GJ, Chambers S, Hoffbrand AV.
The heteroaromatic chelators 1,2-dimethyl-3-hydroxypyrid-4-one,
maltol, mimosine and 2,4-dihydroxypyridine-N-oxide, have been shown
to
mobilize iron from human spleen haemosiderin, ferritin and also from
iron(III) precipitates, all containing equal amounts of iron, at
physiological pH.
In the case of almost every chelator, the least-solubilized
polynuclear iron form was ferritin, whereas haemosiderin was more
soluble and the iron(III) precipitate the most soluble of all.
Most of the chelators were more efficient than desferrioxamine at
releasing iron from ferritin, but less efficient in the removal of
iron from the other two polynuclear iron forms.
It is suggested that the chelator differences in iron mobilization
may
be related to variations in the chelator molecular structure, the
protein structure, iron forms and in the mechanism of iron release.

PMID: 3566714

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/634q5a

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk