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[hormoneman]

NtBHA = N-tert-Butyl hydroxylamine HCl (100%)

or


PBN = (N-tert-Butyl--phenylnitrone) (99+%)

and why or why not

I'm seriously thinking about adding them to my life extension regimen

[tintinet]

I take NtBHA. Why:

See Morelife.org references: Morelife.org NtBHA References



Notably:

1."The use of N-hydroxylamine also avoids the benzaldehyde formed when PBN (-phenyl-N-t-butyl nitrone) decomposes." (by hydrolysis, see below)

"Benzaldehyde is both mutagenicR and carcinogenicR, ... was without effect, and in high concentrations, was toxic to the cells."R
"Chronic benzaldehyde exposure is known to cause central nervous system (CNS) disturbances. Previous studies have shown that benzaldehyde causes the formation of reactive oxygen species (ROS) in rat synaptosomal fractions. Benzaldehyde has also been implicated in ROS formation in the CNS of rats treated with toluene. We have found that benzaldehyde effectively inactivates the antioxidant enzyme glutathione peroxidase ... Since glutathione peroxidase is the main enzyme responsible for removal of hydrogen peroxide and organic hydroperoxides in brain, its inactivation by benzaldehyde may be a main contributor to the observed ROS formation and the observed neurotoxicity caused by either benzaldehyde or toluene exposure. See refs.

2."When fed to rats, PBN (a spin trap) was shown to be an alternative to lipoic acid as a mitochondrial antioxidant. We showed that its breakdown product, NtBHA, was much more active than PBN in vitro.R When we tested its biological activity in vivo, we found it reversed the age-related decline in food consumption and ambulatory activity in rats, although it is not clear which of the two parameters is primarily affected. ... In our present study, we found that NtBHA fed to old rats improves the mitochondrial RCR, prevents the loss of GDH, and decreases glutathione-mixed disulfides in proteins from liver. On the other hand, NtBHA showed no significant effect on liver mitochondria of young rats, even though the dose these rats were receiving was 40% higher than the old rats (as the young consume more water). These observations suggest that NtBHA acts partly as an antioxidant that protects mitochondria and proteins from oxidative damage. See refs.

3. "-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 microM compared with 200 microM PBN to produce a similar effect, suggesting that N-t-butyl hydroxylamine is the active form of PBN. N-Benzyl hydroxylamine and N-methyl hydroxylamine compounds unrelated to PBN were also effective in delaying senescence, suggesting the active functional group is the N-hydroxylamine. See refs.

Edited by tintinet, 26 February 2007 - 09:04 AM.