Sl. Shofer et al., EFFECTS OF HYPOXIA AND TOXICANT EXPOSURE ON ARGININE KINASE FUNCTION AS MEASURED BY P-31-NMR MAGNETIZATION-TRANSFER IN LIVING ABALONE, Comparative biochemistry and physiology. Part C, Pharmacology toxicology & endocrinology, 117(3), 1997, pp. 283-289
The activity of arginine kinase (AK) was evaluated by saturation trans
fer NMR in red abalone (Haliotis rufescens) in response to hypoxia, so
dium azide (NaN3; an inhibitor of cytochrome c oxidase), or penta-chlo
rophenol (PCP; an uncoupler of oxidative phosphorylation) exposure. Ps
eudo-first order rate constants (K-for) in the forward (ATP forming) r
eaction direction showed maximal increases from basal values of 0.025
s(-1) to 0.095, 0.114, 0.126 s(-1) for NaN3 hypoxia, and PCP exposures
, respectively. Increases in K-for were inversely correlated (r(2) = 1
.00) to declines in ATP concentration in all exposed animals. Flux (th
e product of K-for, and phosphoarginine concentration) appeared to con
verge on a common value, from basal flux values of 0.257 mM PA s(-1) t
o 0.703, 0.770, and 0.627 mM PA s(-1) for NaN3, hypoxia, and PCP expos
ures, respectively. It seems likely that all three stresses were equal
ly effective at inhibiting mitochondrial ATP formation, which may acco
unt for the similarity in flux increase, possibly to maximal rates of
AK-mediated ATP formation. Differences in K-for, are related to declin
es in ATP concentrations, which appear to be stress specific, and like
ly indicate additional mechanisms of toxicity for NaN3 and PCP. (C) 19
97 Elsevier Science Inc.