Cd. Smith et al., BRAIN CREATINE-KINASE WITH AGING IN F344 RATS - ANALYSIS BY SATURATION-TRANSFER MAGNETIC-RESONANCE SPECTROSCOPY, Neurobiology of aging, 18(6), 1997, pp. 617-622
We measured in vivo forward flux of the creatine kinase reaction in ra
t forebrain in young (Y: 6 month, n = 13), mid-aged (M: 12 month, n =
7) and aged (O: 27 month, n = 10) animals using 31P magnetic resonance
saturation transfer. Forward flux was reduced in the aged rats (Y: 0.
42 +/- 0.08; M: 0.41 +/- 0.10; O: 0.31 +/- 0.03 s(-1) +/- SD; p = 0.00
8 O vs. Y). In vitro studies in a subset of the same rats showed a par
allel decline in CK activity (Y: 2.16 +/- 0.40; M: 2.17 +/- 0.25; O: 1
.56 +/- 0.06 IU +/- S.D.; p = 0.002 O vs. Y). The in vivo spectroscopi
c and in vitro biochemical measures were significantly correlated. Red
uced creatine kinase activity could account for the observed decreased
forward flux in aging brain. Intracellular pH, phosphocreatine/inorga
nic phosphate ratio, and phospocreatine/gamma-adenosine triphosphate r
atio did not differ between groups. Forward flux may represent a bette
r measure of brain energy function than relative phosphocreatine or ad
enosine triphosphate levels observable in vivo. (C) 1997 Elsevier Scie
nce Inc.