P-31-NMR ANALYSIS OF LETHAL AND SUBLETHAL LESIONS PRODUCED BY KCL-INTOXICATION IN THE ZEBRA MUSSEL, DREISSENA-POLYMORPHA

Noninvasive phosphorus-31 nuclear magnetic resonance spectroscopy (P-3 1-NMR) was utilized to investigate the mechanism of potassium chloride (KCl) toxicity in zebra mussels. P-31-NMR spectra showed several bioe nergetically important high energy phosphates, including ATP, ADP, pho sphoarginine, and inorganic phosphate. Exposure of mussels to 8.6 mM K Cl caused changes in these metabolites and proved lethal to the mussel s when exposed over a 24 h period. This result matched that of the mol luscicide Bayluscide. Here, losses in phosphoarginine and ATP were acc ompanied by a rise in inorganic phosphate and a shift toward intracell ular acidosis. KCl levels below 8.6 mM caused marked changes in mussel high energy phosphates and pH(i). However, these changes were reversi ble once mussels were returned to fresh standard reference water (SRW) . In contrast, mussels exposed to 8.6 mM KCl under hyperbaric conditio ns (20 mg/L O-2) survived during the 24 h KCl exposure and showed norm al ATP peaks and pH(i). The latter mussels, however, died when O-2 sup plementation was removed and mussels were transferred to SRW. Exposure to hypoxic conditions (<1.5 mg/LO(2)) resulted in loss of ATP and red uction in pH(i) similar to that produced to exposure to 8.6 mM KCl. Th e effect-of KCl on ciliary beating within the zebra mussel gills was a lso examined. Ciliary beating stopped in all mussels receiving treatme nt with KCl including those jointly exposed to 8.6 mM KCl and elevated O-2 (20 mg/L). However, ciliary beating resumed in mussels exposed to KCl concentrations less than 4.3 mM when the mussels were transferred to clean SRW. Ciliary beating was not affected by exposure to hypoxic conditions or to elevated O-2 alone. These data suggest: (1) cessatio n of ciliary beat is a specific response to potassium intoxication but is insufficient to cause mussel death; (2) two levels of potassium-in duced injury were observed and were dependent upon the concentration o f potassium to which mussels were exposed. Exposure to KCl below 4.3 m M resulted in reversible alterations of gill physiology while exposure to-concentrations above 4.3 mM resulted in permanent lesions from whi ch recovery was not possible. (C) 1996 Wiley-Liss, Inc.