Abstract
The sensitivity of two measures of tissue energy metabolism to environmental stress was examined in the present study through chronic exposure of crayfish to low concentrations of cadmium. Freshwater crayfish, Procambarus acutus acutus, were exposed to 5 and 10 μ Cd · 1 (as CdCl2) under flow-through conditions for a period of 21 days. After 1, 7, 14, and 21 days of exposure, gill and dorsal muscle tissue samples were collected to determine Cd and Zn content. phosphoadenylate (ATP, ADP and AMP) concentrations and gill tissue respiration rates. Two potential sublethal stress indicators, the adenylate energy charge [AEC = (ATP + 1/2 ADP)/ (ATP + ADP + AMP)] and ATP turnover rate were calculated. Cd was observed to concentrate over time in gills, but not in muscle tissue. No evidence was found to indicate replacment of Zn by Cd in the tissues analyzed. In addition, Cd tissue concentrations were not correlated (p > 0.05) with phosphoadenylate concentrations or respiration rate. After seven days exposure, ATP and total phosphoadenylate concentrations in gill tissue were significantly (p < 0.05) lower in crayfish exposed to Cd. This decrease was associated with lower gill tissue respiration rates, probably due to enzyme dysfunction caused by Cd. The return of ATP concentrations and gill tissue respiration rates to control values observed after day 7 may be associated with the induction of replacement enzymes and metallothioneins stimulated by Cd. ATP turnover rate (based on 1 mole O2 ← 6 moles ATP) in gill tissue was not correlated (p > 0.05) with the two measures of aerobic respiration recorded, and was not considered to represent an accurate indication of cellular energy turnover. In contrast to an earlier study utilizing a different crayfish species, no significant (p > 0.05) decreases in tissue AEC were observed in the present study in crayfish exposed to Cd. The absence of AEC changes under the exposure conditions imposed in this investigation could be related to life history differences or in species specific sensitivity to the toxic effects of Cd. Under the experimental conditions utilized, the adenylate energy charge and ATP turnover rate did not provide indications of Cd toxicity at lower concentrations than those previously determined through conventional chronic lethality testing. However, these physiological indicators did permit a more complete understanding of the toxic action of cadmium on the tissues examined.
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