From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Mon Nov 02 1998 - 09:55:55 MST
The Journal of Neuroscience 18(19): 8047-8055 October 1,1998
"Long-Term Dietary Strawberry, Spinach, or Vitamin E Supplementation
Retards the Onset of Age-Related Neuronal Signal-Transduction and Cognitive
Behavioral Deficits"
Abstract:
Recent research has indicated that increased vulnerability to oxidative
stress may be the major factor involved in CNS functional declines in aging
and age-related neurodegenerative diseases, and that antioxidants, e.g.,
vitamin E, may ameliorate or prevent these declines. Present studies
examined whether long-term feeding of Fischer 344 rats, beginning when the
rats were 6 months of age and continuing for 8 months, with diets
supplemented with a fruit or vegetable extract identified as being high in
antioxidant activity, could prevent the age-related induction of
receptor-meduated signal transduction deficits that might have a behavioral
component. Thus, the following parameters were examined: (1)
oxotremorine-enhanced striatal dopamine release (OX-K+-ERDA), (2)
cerebellar B receptor augmeentation of GABA responding, (3) striatal
synaptosomal 45Ca2+ clearance, (4) carbachol-stimulated GTPase activity,
and (5) Morris water maze peformance. The rats were given control diets or
those supplemented with strawberry extracts (SE), 9.5 gm/kg dried aqueous
extract (DAE), spinach (SPN 6.4 gm/kg DAE), or vitamin E (500 IU/kg).
Results indicated that SPN-fed rats demontrated the greatest retardation of
age-effects on all parameters except GTPase acitivity, on which SE had the
greatest effect, whereas SE and Vitamin Eshowed signifcant but equal
protection against these age-induced deficits on the other parameters. For
example, OX-K+-ERDA enhancement was four times greater in the SPN group
than in controls. Thus, phytochemicals present in antioxidant-rich foods
such as spinach may be beneficial in retarding functional age-related CNS
and cognitive behavioral deficits and, perhaps, may have some benefit in
neurodegenerative disease.
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