This study was undertaken to investigate whether the accumulation of end products of anaerobic metabolism can be used as an early indicator of deteriorating conditions during transport of live abalone Haliotis midae. A first series of experiments revealed that the enzyme tauropine dehydrogenase, responsible for the production of tauropine, is present in high activities (54 U g wet weight−1) in the shell adductor muscle, but D-lactate dehydrogenase, responsible for the production of D-lactate, is the predominantly active enzyme (10 U g wet weight−1) in foot muscle. The next series of experiments investigated the potential of anaerobic metabolism in the abalone by subjecting the gastropod to either functional anoxia (exercise metabolism) or 6 h of environmental anoxia (seawater gassed with nitrogen). Exercise, primarily powered by the shell adductor muscle, was mainly fueled by glycolysis resulting in the production of tauropine, whereas during 6 h of experimental anoxia, fermentation of glycogen led to the formation of mainly tauropine in the shell adductor muscle and mainly D-lactate in the foot muscle. The last experiment, investigating changes in these metabolites during simulated (abalone packed in oxygen-filled plastic bags resting on foam sponges soaked in seawater) transportation stress of up to 36 h at 7 and 10°C, clearly showed that tauropine accumulation in the shell adductor muscle and D-lactate accumulation in the foot muscle is time-dependent. Both metabolites are already produced during the first 6 h of simulated transportation (especially at 10°C), indicating that aerobic metabolism is impaired at an early stage of transportation. Hence, these metabolites can serve as indicators of the conditions abalone were subjected to during transport. Furthermore, abalone use the strategy of metabolic depression in this simulation experiment, as indicated by the decreased glycolytic flux in various tissues.
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