Long-term dietary strawberry, spinach, or vitamin E supplementation retards the onset of age-related neuronal signal-transduction and cognitive behavioral deficits.
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-mediated 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 beta receptor augmentation of GABA responding, (3) striatal synaptosomal 45Ca2+ clearance, (4) carbachol-stimulated GTPase activity, and (5) Morris water maze performance. 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 demonstrated the greatest retardation of age-effects on all parameters except GTPase activity, on which SE had the greatest effect, whereas SE and vitamin E showed significant 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.
Joseph
J A
JA
United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts, Boston, Massachusetts 02111, USA.
Shukitt-Hale
B
B
Denisova
N A
NA
Prior
R L
RL
Cao
G
G
Martin
A
A
Taglialatela
G
G
Bickford
P C
PC
D000375:Aging / Q000502:physiology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001835:Body Weight; D001923:Brain Chemistry / Q000502:physiology; D002132:Calcium Radioisotopes; D003072:Cognition Disorders / Q000178:diet therapy*; D003342:Corpus Striatum / Q000737:chemistry / Q000378:metabolism; D004032:Diet; D004298:Dopamine / Q000378:metabolism; D004435:Eating; D004594:Electrophysiology; D005638:Fruit; D020558:GTP Phosphohydrolases / Q000378:metabolism; D008297:Male; D009638:Norepinephrine / Q000502:physiology; D011689:Purkinje Cells / Q000737:chemistry / Q000201:enzymology; D051381:Rats; D011916:Rats, Inbred F344; D017382:Reactive Oxygen Species / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects*; D018724:Spinacia oleracea; D013574:Synaptosomes / Q000737:chemistry / Q000201:enzymology; D013997:Time Factors; D014810:Vitamin E / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000032:analysis / Q000502:physiology
D000975:Antioxidants; D002132:Calcium Radioisotopes; D017382:Reactive Oxygen Species; D014810:Vitamin E; D005680:gamma-Aminobutyric Acid; D020558:GTP Phosphohydrolases; D004298:Dopamine; D009638:Norepinephrine