Geronova has some excellent prices on PBN and TBHA now. PBN $175/25g and TBHA(NtBHA) about the same. So for PBN, at a very conservative 10mg/day, that is almost a 7 year supply.
LongeCityAdvocacy & Research for Unlimited Lifespans
PBN--really low prices
Started by
lynx
, Nov 24 2004 05:05 AM
8 replies to this topic
#3
-
- Guest
- 1,207 posts
- -3 ₮
- Location:Arizona, Los Angles, San Diego, so many road
Posted 26 November 2004 - 05:16 PM
lynx,
I am always interested in the new...
Educate us: how do these work, and are they safe?
Thanks, it's good to see you posting around.
Hey lynx, can you submit a sample of the L-theanine Rizzer recently sent you? I am going to organize this about mid-December; but we need to chat.
Happy Thanksgiving, lynx.
I am always interested in the new...
Educate us: how do these work, and are they safe?
Thanks, it's good to see you posting around.
Hey lynx, can you submit a sample of the L-theanine Rizzer recently sent you? I am going to organize this about mid-December; but we need to chat.
Happy Thanksgiving, lynx.
#4
-
- Guest
- 366 posts
- 2 ₮
Posted 26 November 2004 - 06:45 PM
Dear Nootropi,
First off, let me say that I appreciate your postings-- as I have read through many and have recieved valuable information and insight regarding different supplements.
It seems as though you have altered your attitude to a certain extent over the past few months, but some individuals want to continue beating the dead horse. It is unfortunate that you no longer want to post at the Avant Labs forum, I hope you reconsider.
Secondly, the price of PBN as I've seen it before is about $20 a gram. So this price which Lynx is quoting is absoultely remarkable. I wonder if Rizzer would carry this stuff?
Anyway, here are some abstracts for you regarding PBN.
Get ready for some major reading . [thumb]
PBN (aka N-tert-butyl-alpha-phenylnitrone):
Biosci Biotechnol Biochem 1998 Apr;62(4):792-4 Related Articles, Books
A spin trap, N-tert-butyl-alpha-phenylnitrone extends the life span of
mice.
Saito K, Yoshioka H, Cutler RG
Gerontology Research Center, National Institute on Aging, NIH,
Baltimore, MD 21224, USA.
To characterize the pharmacological effects of
N-tert-butyl-alpha-phenylnitrone (PBN) on life span, we administered PBN
in drinking water to 24.5-month-old mice, and the survivors were
counted. Their water consumption and body weights were measured as
biological markers. PBN-treated animals as compared with control animals
had prolonged mean and maximum life spans. Their water consumption
decreased but no significant change was found in their body weights,
indicating that the metabolism was improved. Results showed that PBN
indeed affects physiological functions and extends life span. We propose
that nitric oxide release from PBN may be involved in altering the aging
process.
---
Arch Biochem Biophys 1995 Dec 20;324(2):249-54
Effect of the spin-trapping compound N-tert-butyl-alpha-phenylnitrone on protein
oxidation and life span.
Dubey A, Forster MJ, Sohal RS
UI: 96132652
---
J Biol Chem 2000 Mar 10;275(10):6741-6748
N-t-Butyl Hydroxylamine, a Hydrolysis Product of alpha-Phenyl-N-t-butyl
Nitrone, Is More Potent in Delaying Senescence in Human Lung Fibroblasts.
Atamna H, Paler-Martinez A, Ames BN
Division of Biochemistry and Molecular Biology, Department of Molecular and
Cell Biology, University of California, Berkeley, California 94720-3202.
alpha-Phenyl-N-t-butyl nitrone (PBN), a spin trap, scavenges hydroxyl
radicals, protects tissues from oxidative injury, and delays senescence of
both normal human lung fibroblasts (IMR90) and senescence-accelerated mice.
N-t-butyl hydroxylamine and benzaldehyde are the breakdown products of PBN.
N-t-Butyl hydroxylamine delays senescence of IMR90 cells at concentrations as
low as 10 muM compared with 200 muM PBN to produce a similar effect, suggestin
g that N-t-butyl hydroxylamine is the active form of PBN. N-Benzyl hydroxylami
ne and N-methyl hydroxylamine compounds unrelated to PBN were also effective i
n delaying senescence, suggesting the active functional group is the N-hydroxy
lamine. All the N-hydroxylamines tested significantly decreased the endogenous
production of oxidants, as measured by the oxidation of 2',7'-dichlorodihydro
fluorescin and the increase in the GSH/GSSG ratio. The acceleration of senesce
nce induced by hydrogen peroxide is reversed by the N-hydroxylamines. DNA dama
ge, as determined by the level of apurinic/apyrimidinic sites, also decreased
significantly follong treatment with N-hydroxylamines. The N-hydroxylamines
appear to be efftive through mitochondria; they delay age-dependent changes in
mitochondr as measured by accumulation of rhodamine-123, they prevent
reduction of tochrome C(FeIII) by superoxide radical, and they reverse an
age-dependent cay of mitochondrial aconitase, suggesting they react with the
superoxide radical.
----
Carney JM Floyd RA
Protection against oxidative damage to CNS by alpha-phenyl-
tert-butyl nitrone (PBN) and other spin-trapping agents: a
novel series of nonlipid free radical scavengers.
In: J Mol Neurosci (1991) 3(1):47-57
Brain is extremely susceptible to oxidative damage. Utilizing
a series of novel approaches, we have demonstrated that
oxidative damage occurs during an ischemia/reperfusion
insult (IRI) to brain. Thus, we have demonstrated that an
IRI to Mongolian gerbil brain results in: (1) an enhanced
rate of salicylate hydroxylation, implicating an increased
flux of hydroxyl free radicals; (2) an enhanced flux of
free radicals as determined by spin-trapping; (3) an
enhanced level of endogenous protein oxidation; (4) a
decrease in glutamine synthetase (GS) activity, an enzyme
very sensitive to oxidative damage; and (5) demonstration
of protection from an IRI by administering the spin-
trapping agent alpha-phenyl-tert-butyl nitrone
(PBN). The novel observation that PBN offers protection
from the lethality brought on by a brain IRI appears to be
clearly linked to the ability of the administered spin-trap
to inhibit oxidative damage as evidenced by the decreased
amount of brain protein oxidation and the prevention of an
IRI-mediated loss of GS activity in treated
animals. Aged gerbils are more sensitive to the lethal
action of a brain IRI than younger animals, but they are
protected by PBN administration as are the younger animals.
Older gerbils have a significantly higher level of oxidized
protein in the brain. Older gerbils have decreased
activities of GS and neutral protease, the
enzyme that removes oxidized protein, than younger animals.
Chronic twice daily administration of PBN (32 mg/kg) for 14
days to older animals significantly lowered brain oxidized
protein levels and raised GS and neutral protease activity
to those observed in younger animals. Cessation of PBN
administration resulted in a time-dependent
restoration of protein oxidation levels and enzyme
activities back to those observed prior to spin-trap
administration. Older gerbils exhibit significantly higher
errors in a radial arm maze than younger
animals, but older gerbils that had received chronic daily
treatments of PBN (32 mg/kg) for 14 days committed
significantly less errors than untreated controls. The
errors committed in PBN-treated animals
was decreased down to the level of those observed in
younger animals.
Clearly the spin-trapping agent, PBN, appears to have
promise in: (1)elucidation of the role of oxidative damage
in normal brain function during aging, (2) understanding
the development of pathological conditions, and (3)
development of treatment regimens for prevention
of damage that occurs during the development of
pathological conditions and in aging.
----
Authors
Hagen TM. Wehr CM. Ames BN.
Institution
Department of Molecular and Cell Biology, University of California at
Berkeley 94720, USA. tory.hagen@orst.edu
Title
Mitochondrial decay in aging. Reversal
through supplementation of acetyl-L-carnitine and
N-tert-butyl-alpha-phenyl-nitrone.
Source
Annals of the New York Academy of Sciences. 854:214-23, 1998 Nov 20.
Abstract
We show that mitochondrial function in the majority of
hepatocytes isolated from old rats (24 mo) is significantly impaired.
Mitochondrial membrane potential, cardiolipin levels,
respiratory control ratio, and overall cellular O2 consumption decline, and
the level of oxidants increases. To examine whether dietary supplementation
of micronutrients that may have become essential with age could reverse the
decline in mitochondrial function, we supplemented the diet
of old rats with 1% (w/v) acetyl-L-carnitine (ALCAR) in drinking water. ALCAR
supplementation (1 month) resulted in significant increases in cellular
respiration, mitochondrial membrane potential, and
cardiolipin values. However, supplementation also increased the rate of
oxidant production, indicating that the efficiency of
mitochondrial electron transport had not improved. To
counteract the potential increase in oxidative stress, animals were
administered N-tert-butyl-alpha-phenyl-nitrone (30 mg/kg) (PBN) with or
without ALCAR. Results showed that PBN significantly lowered oxidant
production as measured by 2,7'-dichlorofluorescin diacetate (DCFH), even when
ALCAR was coadministered to the animals. Thus, dietary supplementation with
ALCAR, particularly in combination with PBN, improves
mitochondrial function without a significant increase in
oxidative stress.
----
First off, let me say that I appreciate your postings-- as I have read through many and have recieved valuable information and insight regarding different supplements.
It seems as though you have altered your attitude to a certain extent over the past few months, but some individuals want to continue beating the dead horse. It is unfortunate that you no longer want to post at the Avant Labs forum, I hope you reconsider.
Secondly, the price of PBN as I've seen it before is about $20 a gram. So this price which Lynx is quoting is absoultely remarkable. I wonder if Rizzer would carry this stuff?
Anyway, here are some abstracts for you regarding PBN.
Get ready for some major reading . [thumb]
PBN (aka N-tert-butyl-alpha-phenylnitrone):
Biosci Biotechnol Biochem 1998 Apr;62(4):792-4 Related Articles, Books
A spin trap, N-tert-butyl-alpha-phenylnitrone extends the life span of
mice.
Saito K, Yoshioka H, Cutler RG
Gerontology Research Center, National Institute on Aging, NIH,
Baltimore, MD 21224, USA.
To characterize the pharmacological effects of
N-tert-butyl-alpha-phenylnitrone (PBN) on life span, we administered PBN
in drinking water to 24.5-month-old mice, and the survivors were
counted. Their water consumption and body weights were measured as
biological markers. PBN-treated animals as compared with control animals
had prolonged mean and maximum life spans. Their water consumption
decreased but no significant change was found in their body weights,
indicating that the metabolism was improved. Results showed that PBN
indeed affects physiological functions and extends life span. We propose
that nitric oxide release from PBN may be involved in altering the aging
process.
---
Arch Biochem Biophys 1995 Dec 20;324(2):249-54
Effect of the spin-trapping compound N-tert-butyl-alpha-phenylnitrone on protein
oxidation and life span.
Dubey A, Forster MJ, Sohal RS
UI: 96132652
---
J Biol Chem 2000 Mar 10;275(10):6741-6748
N-t-Butyl Hydroxylamine, a Hydrolysis Product of alpha-Phenyl-N-t-butyl
Nitrone, Is More Potent in Delaying Senescence in Human Lung Fibroblasts.
Atamna H, Paler-Martinez A, Ames BN
Division of Biochemistry and Molecular Biology, Department of Molecular and
Cell Biology, University of California, Berkeley, California 94720-3202.
alpha-Phenyl-N-t-butyl nitrone (PBN), a spin trap, scavenges hydroxyl
radicals, protects tissues from oxidative injury, and delays senescence of
both normal human lung fibroblasts (IMR90) and senescence-accelerated mice.
N-t-butyl hydroxylamine and benzaldehyde are the breakdown products of PBN.
N-t-Butyl hydroxylamine delays senescence of IMR90 cells at concentrations as
low as 10 muM compared with 200 muM PBN to produce a similar effect, suggestin
g that N-t-butyl hydroxylamine is the active form of PBN. N-Benzyl hydroxylami
ne and N-methyl hydroxylamine compounds unrelated to PBN were also effective i
n delaying senescence, suggesting the active functional group is the N-hydroxy
lamine. All the N-hydroxylamines tested significantly decreased the endogenous
production of oxidants, as measured by the oxidation of 2',7'-dichlorodihydro
fluorescin and the increase in the GSH/GSSG ratio. The acceleration of senesce
nce induced by hydrogen peroxide is reversed by the N-hydroxylamines. DNA dama
ge, as determined by the level of apurinic/apyrimidinic sites, also decreased
significantly follong treatment with N-hydroxylamines. The N-hydroxylamines
appear to be efftive through mitochondria; they delay age-dependent changes in
mitochondr as measured by accumulation of rhodamine-123, they prevent
reduction of tochrome C(FeIII) by superoxide radical, and they reverse an
age-dependent cay of mitochondrial aconitase, suggesting they react with the
superoxide radical.
----
Carney JM Floyd RA
Protection against oxidative damage to CNS by alpha-phenyl-
tert-butyl nitrone (PBN) and other spin-trapping agents: a
novel series of nonlipid free radical scavengers.
In: J Mol Neurosci (1991) 3(1):47-57
Brain is extremely susceptible to oxidative damage. Utilizing
a series of novel approaches, we have demonstrated that
oxidative damage occurs during an ischemia/reperfusion
insult (IRI) to brain. Thus, we have demonstrated that an
IRI to Mongolian gerbil brain results in: (1) an enhanced
rate of salicylate hydroxylation, implicating an increased
flux of hydroxyl free radicals; (2) an enhanced flux of
free radicals as determined by spin-trapping; (3) an
enhanced level of endogenous protein oxidation; (4) a
decrease in glutamine synthetase (GS) activity, an enzyme
very sensitive to oxidative damage; and (5) demonstration
of protection from an IRI by administering the spin-
trapping agent alpha-phenyl-tert-butyl nitrone
(PBN). The novel observation that PBN offers protection
from the lethality brought on by a brain IRI appears to be
clearly linked to the ability of the administered spin-trap
to inhibit oxidative damage as evidenced by the decreased
amount of brain protein oxidation and the prevention of an
IRI-mediated loss of GS activity in treated
animals. Aged gerbils are more sensitive to the lethal
action of a brain IRI than younger animals, but they are
protected by PBN administration as are the younger animals.
Older gerbils have a significantly higher level of oxidized
protein in the brain. Older gerbils have decreased
activities of GS and neutral protease, the
enzyme that removes oxidized protein, than younger animals.
Chronic twice daily administration of PBN (32 mg/kg) for 14
days to older animals significantly lowered brain oxidized
protein levels and raised GS and neutral protease activity
to those observed in younger animals. Cessation of PBN
administration resulted in a time-dependent
restoration of protein oxidation levels and enzyme
activities back to those observed prior to spin-trap
administration. Older gerbils exhibit significantly higher
errors in a radial arm maze than younger
animals, but older gerbils that had received chronic daily
treatments of PBN (32 mg/kg) for 14 days committed
significantly less errors than untreated controls. The
errors committed in PBN-treated animals
was decreased down to the level of those observed in
younger animals.
Clearly the spin-trapping agent, PBN, appears to have
promise in: (1)elucidation of the role of oxidative damage
in normal brain function during aging, (2) understanding
the development of pathological conditions, and (3)
development of treatment regimens for prevention
of damage that occurs during the development of
pathological conditions and in aging.
----
Authors
Hagen TM. Wehr CM. Ames BN.
Institution
Department of Molecular and Cell Biology, University of California at
Berkeley 94720, USA. tory.hagen@orst.edu
Title
Mitochondrial decay in aging. Reversal
through supplementation of acetyl-L-carnitine and
N-tert-butyl-alpha-phenyl-nitrone.
Source
Annals of the New York Academy of Sciences. 854:214-23, 1998 Nov 20.
Abstract
We show that mitochondrial function in the majority of
hepatocytes isolated from old rats (24 mo) is significantly impaired.
Mitochondrial membrane potential, cardiolipin levels,
respiratory control ratio, and overall cellular O2 consumption decline, and
the level of oxidants increases. To examine whether dietary supplementation
of micronutrients that may have become essential with age could reverse the
decline in mitochondrial function, we supplemented the diet
of old rats with 1% (w/v) acetyl-L-carnitine (ALCAR) in drinking water. ALCAR
supplementation (1 month) resulted in significant increases in cellular
respiration, mitochondrial membrane potential, and
cardiolipin values. However, supplementation also increased the rate of
oxidant production, indicating that the efficiency of
mitochondrial electron transport had not improved. To
counteract the potential increase in oxidative stress, animals were
administered N-tert-butyl-alpha-phenyl-nitrone (30 mg/kg) (PBN) with or
without ALCAR. Results showed that PBN significantly lowered oxidant
production as measured by 2,7'-dichlorofluorescin diacetate (DCFH), even when
ALCAR was coadministered to the animals. Thus, dietary supplementation with
ALCAR, particularly in combination with PBN, improves
mitochondrial function without a significant increase in
oxidative stress.
----
#6
- Topic Starter
-
- Guest
- 643 posts
- 5 ₮
Posted 26 November 2004 - 09:52 PM
Yes, they could be used instead of R-ALA, but the inclusion of R-ALA is useful in ways that PBN/NtBHA are not.
First, sulfur anti-oxidants have effects that can't easily be duplicated by molecules without sulfur.
Second, ALA raises glutathione.
Third, ALA improves insulin sensitivity, thus reducing circulating glucose, which increases BDNF and limits protein glycation.
Fourth, Lipoic acid is necessary for some parts of The Citric Acid cycle.
Fifth, ALA is a chelator of heavy metals.
Sixth, Lipoic acid recycles Vit C & E.
Seventh, Lipoic acid is water/fat soluble, giving it unique scope.
and there are more that I can't think of now.
First, sulfur anti-oxidants have effects that can't easily be duplicated by molecules without sulfur.
Second, ALA raises glutathione.
Third, ALA improves insulin sensitivity, thus reducing circulating glucose, which increases BDNF and limits protein glycation.
Fourth, Lipoic acid is necessary for some parts of The Citric Acid cycle.
Fifth, ALA is a chelator of heavy metals.
Sixth, Lipoic acid recycles Vit C & E.
Seventh, Lipoic acid is water/fat soluble, giving it unique scope.
and there are more that I can't think of now.
#7
- Topic Starter
-
- Guest
- 643 posts
- 5 ₮
Posted 26 November 2004 - 10:23 PM
lynx,
I am always interested in the new...
Educate us: how do these work, and are they safe?
Thanks, it's good to see you posting around.
Hey lynx, can you submit a sample of the L-theanine Rizzer recently sent you? I am going to organize this about mid-December; but we need to chat.
Happy Thanksgiving, lynx.
I wish it were so easy to say how they work, but I do know that it is more than just anti-oxidant effects.
http://www.anakata.h...ev-123-1021.pdf
Is a pretty good review of the non-antioxidant ways that Nitrones do their magic.
and here is a list of abstracts at Dr. P's website
http://www.nitrone.c...tnf-nitrone.htm
and here is an in depth look at Nitric Oxide and how it can mess you up with mention of Spin Traps inhibiting that.
http://plaza.ufl.edu/cleeuwen/Drew.PDF
and of course the geronova website is a treasure trove, they really know what they are talking about.
Regarding Rizzer and the Theanine, until my last order is completed with a receipt, and some communication in response to numerous emails is recieved, I will not be ordering from him nor encouraging others to do so.
EDIT: changed spin trapping to anti-oxidant effects for obvious reason.
Edited by lynx, 27 November 2004 - 12:44 AM.
#9
- Topic Starter
-
- Guest
- 643 posts
- 5 ₮
Posted 28 November 2004 - 09:56 PM
Here is a great little study that I missed before because they misspelled PBN.
FULL TEXT
http://www.jbc.org/c...276/35/32779#F8
J Biol Chem. 2001 Aug 31;276(35):32779-85. Epub 2001 Jul 03. Related Articles, Links
Induction of neurite outgrowth in PC12 cells by alpha -phenyl-N-tert-butylnitron through activation of protein kinase C and the Ras-extracellular signal-regulated kinase pathway.
Tsuji M, Inanami O, Kuwabara M.
Laboratory of Radiation Biology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan.
The spin trap alpha-phenyl-N-tert-butylnitron (PBN) is widely used for studies of the biological effects of free radicals. We previously reported the protective effects of PBN against ischemia-reperfusion injury in gerbil hippocampus by its activation of extracellular signal-regulated kinase (ERK) and suppression of both stress-activated protein kinase and p38 mitogen-activated protein kinase. In the present study, we found that PBN induced neurite outgrowth accompanied by ERK activation in PC12 cells in a dose-dependent manner. The induction of neurite outgrowth was inhibited significantly not only by transient transfection of PC12 cells with dominant negative Ras, but also by treatment with mitogen-activated protein kinase/ERK kinase inhibitor PD98059. The activation of receptor tyrosine kinase TrkA was not involved in PBN-induced neurite outgrowth. A protein kinase C (PKC) inhibitor, GF109203X, was found to inhibit neurite outgrowth. The activation of PKCepsilon was observed after PBN stimulation. PBN-induced neurite outgrowth and ERK activation were counteracted by the thiol-based antioxidant N-acetylcysteine. From these results, it was concluded that PBN induced neurite outgrowth in PC12 cells through activation of the Ras-ERK pathway and PKC.
PMID: 11438521 [PubMed - indexed for MEDLINE]
FULL TEXT
http://www.jbc.org/c...276/35/32779#F8
In conclusion, we demonstrated here that PBN, a spin trap, could induce neurite outgrowth of PC12 cells in a dose-dependent manner. PBN-induced neurite outgrowth was mediated by the activation of ERK. The activation of Ras was critical, but unlike NGF, PBN did not cause activation of the TrkA receptor tyrosine kinase and subsequent activation of Shc, PI3-kinase, and PLC. PBN activated PKC. The activation of PKC was necessary for neurite outgrowth induced by PBN, although the activation of PKC was not involved in ERK activation. A thiol-based antioxidant, NAC, inhibited PBN-induced neurite outgrowth in a dose-dependent manner, and not only NAC but also other SH-reducing agents could inhibit PBN-induced phosphorylation of ERK. These data suggest that PBN induces neurite outgrowth through activation of the Ras-ERK pathway and PKC.
0 user(s) are reading this topic
0 members, 0 guests, 0 anonymous users
