X-Message-Number: 11690
Date: Thu, 06 May 1999 15:01:17 -0700
From: Olaf Henny <>
Subject: PBN May Have Use in Restoring Ischemic Damage

A posting by Peter H. Proctor in sci.life-extension, which told of
extension of mean and maximum lifspan in mice after adding PBN to their
drinking water prompted me to look it up in Medline.

A couple of abstracts sprang up, that indicated, that PBN may have a use in
reducing some ischemic damage, as well as restoring some mitochondrial
function if administered in conjunction with acetyl-L-carnitine.




 Synonyms: Phenyl N-tert-butylnitrone; PBN; 2-Propanamine,
2-methyl-N-(phenylmethylene)-, N-oxide


N-tert-butyl-alpha-phenylnitrone reduces the number of
microinfarctions in the rabbit brain cortex.

Roos MW, Ericsson A

Department of Physiology, BMC, Uppsala University, Sweden. 

Dementia due to cerebral ischemic lesions is relatively common in the
elderly. Since many of these lesions are probably caused by emboli,
studying emboli-induced cerebral lesions in rabbits should, hopefully,
provide information that is useful when searching for a means of preventing
and treating vascular dementia in humans. Using magnetic resonance imaging
we have found that N-tert-butyl-alpha-phenyl-nitrone (a free radical
scavenger) reduced the number of emboli-induced cerebral microinfarctions
in the rabbit cortex but did not have any impact on the number of
infarctions found in the subcortical structures. The results suggest that
significant amount of free radicals are produced in the ischemic foci
located in the cortex, but not in the ischemic foci located in the
subcortical structures. This finding may be of importance when considering
treatments for cerebral ischemia in humans. 

PMID: 9928850, UI: 99125930 

Hagen TM, Wehr CM, Ames BN

Department of Molecular and Cell Biology, University of California at
Berkeley 94720, USA.

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. 

PMID: 9928432, UI: 99127393 

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