Effect of Aminotransferase Inhibitors on the Pattern of Free Amino Acid Accumulation in Isolated Mussel Hearts Subjected to Hyperosmotic Stress

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Abstract
Ventricles isolated from mussels adapted at 12 ‰ artificial seawater (ASW) were incubated in 12 ‰ and 32 ‰ ASW for 8 h in the presence and absence of the aminotransferase inhibitors, aminooxyacetic acid (AOA) and L-cycloserine (L-CS). The aminotransferase inhibitors at 1 mM did not affect oxygen uptake or heartbeat recovery in isolated ventricles during high salinity adaptation (12 ‰ ASW → 32 ‰ ASW). Alanine-glyoxylate, glutamate-pyruvate, glutamate-oxaloacetate, and ornithine-α-ketoglutarate aminotransferase activities from the mussel ventricles had between 10⁻⁷ M and 10⁻⁵ M with AOA and between 10⁻⁶ M and 5 X 10⁻⁴ M with L-CS. Tissues incubated with no inhibitor at 32 ‰ showed no change in taurine levels and a 70% increase in the total free amino acid pool size (excluding taurine) over tissues incubated at 12 ‰. This increase at 32 ‰ was due to sharp rises in alanine, proline, and β-alanine levels. In comparing the amino acid pool sizes in tissues incubated with or without inhibitor, addition of AOA had the following effects: (1) no change in the total average pool size at 12 ‰ and only a slight or insignificant decrease in the total average pool size at 32 ‰, (2) a decrease of 88% and 60% in the respective proline and alanine levels at 32 ‰, (3) no change in the β-alanine or taurine levels, (4) a large increase in the ornithine level at 32 ‰, and (5) smaller redistributions in the concentrations of the other amino acids at both salinities. It appears that the proline and alanine which accumulate during hyperosmotic shock are produced primarily through transaminase linked pathways. Additionally, the absence of a marked inhibition by AOA of the increase in the total average free amino acid pool size after hyperosmotic shock seems indicative of an accumulation of the products of protein and phosphoarginine catabolism.