The biotic ligand model (BLM) is a mechanistic approach that greatly improves our ability to generate site-specific ambient water quality criteria (AWQC)for metals in the natural environment relative to conventional relationships based only on hardness. The model is flexible; all aspects of water chemistry that affect toxicity can be included, so the BLM integrates the concept of bioavailability into AWQC--in essence the computational equivalent of water effect ratio (WER) testing. The theory of the BLM evolved from the gill surface interaction model (GSIM) and the free ion activity model (FIAM). Using an equilibrium geochemical modeling framework, the BLM incorporates the competition of the free metal ion with other naturally occurring cations (e.g., Ca2+, Na+, Mg2-, H+), togetherwith complexation by abiotic ligands [e.g., DOM (dissolved organic matter), chloride, carbonates, sulfide] for binding with the biotic ligand, the site of toxic action on the organism. On the basis of fish gill research, the biotic ligands appear to be active ion uptake pathways (e.g., Na+ transporters for copper and silver, Ca2+ transporters for zinc, cadmium, lead, and cobalt), whose geochemical characteristics (affinity = log K, capacity = Bmax) can be quantified in short-term (3-24 h) in vivo gill binding tests. In general, the greater the toxicity of a particular metal, the higher the log K. The BLM quantitatively relates short-term binding to acute toxicity, with the LA50 (lethal accumulation) being predictive of the LC50 (generally 96 h for fish, 48 h for daphnids). We critically evaluate currently available BLMs for copper, silver, zinc, and nickel and gill binding approaches for cadmium, lead, and cobalt on which BLMs could be based. Most BLMs originate from tests with fish and have been recalibrated for more sensitive daphnids by adjustment of LA50 so as to fit the results of toxicity testing. Issues of concern include the arbitrary nature of LA50 adjustments; possible mechanistic differences between daphnids and fish that may alter log K values, particularly for hardness cations (Ca2+, Mg2+); assumption of fixed biotic ligand characteristics in the face of evidence that they may change in response to acclimation and diet; difficulties in dealing with DOM and incorporating its heterogeneity into the modeling framework; and the paucity of validation exercises on natural water data sets. Important needs include characterization of biotic ligand properties at the molecular level; development of in vitro BLMs, extension of the BLM approach to a wider range of organisms, to the estuarine and marine environment, and to deal with metal mixtures; and further development of BLM frameworks to predict chronic toxicity and thereby generate chronic AWQC.
Trout fitted with dorsal aortic cannulae were subjected to 6 min of intensive exercise and monitored over the following 12 h recovery period. Delayed mortality was =40%; the majority of deaths occurred 4-8 h post-exercise. Surviving fish exhibited a short-lived haemoconcentration reflected in increased haematocrit, haemoglobin, plasma protein, Na+ and CI-levels; an extended rise in plasma [K+]; a quickly corrected respiratory acidosis;and a more prolonged metabolic acidosis in concert with a rise in blood lactate. Dying fish exhibited very similar trends except for a significantly greater metabolic acidosis, lower plasma [CI-1, and the apparent accumulation of an unknown anion in the blood prior to death. Cardiac failure did not occur. Blood metabolic acid levels, while elevated, were only -50% of peak lactate anion levels and well within the normal range of tolerance, as were all other changes observed in the blood of non-survivors. The hypothesis that post-exercise mortality is due to excessive ' lactic acid ' accumulation in the blood is discounted. It is suggested that intracellular acidosis may be the proximate cause of death.
SummaryAmmonia excretion at the gills of fish has been studied for 80 years, but the mechanism(s) involved remain controversial. The relatively recent discovery of the ammonia-transporting function of the Rhesus (Rh) proteins, a family related to the Mep/Amt family of methyl ammonia and ammonia transporters in bacteria, yeast and plants, and the occurrence of these genes and glycosylated proteins in fish gills has opened a new paradigm. We provide background on the evolution and function of the Rh proteins, and review recent studies employing molecular physiology which demonstrate their important contribution to branchial ammonia efflux. Rhag occurs in red blood cells, whereas several isoforms of both Rhbg and Rhcg occur in many tissues. In the branchial epithelium, Rhcg appears to be localized in apical membranes and Rhbg in basolateral membranes. Their gene expression is upregulated during exposure to high environmental ammonia or internal ammonia infusion, and may be sensitive to synergistic stimulation by ammonia and cortisol. Rhcg in particular appears to be coupled to H + excretion and Na + uptake mechanisms. We propose a new model for ammonia excretion in freshwater fish and its variable linkage to Na + uptake and acid excretion. In this model, Rhag facilitates NH 3 flux out of the erythrocyte, Rhbg moves it across the basolateral membrane of the branchial ionocyte, and an apical "Na THE JOURNAL OF EXPERIMENTAL BIOLOGY 2304and helps to explain some of the discrepancies in the earlier literature. Retrospection on past controversiesSince the classic divided chamber experiments of Homer Smith (Smith, 1929), it has been known that freshwater fish excrete their nitrogen waste predominantly as ammonia through the gills. August Krogh (Krogh, 1939) presented circumstantial evidence that ammonia excretion is in some way linked to active Na + uptake at the gills of freshwater animals. Jean Maetz (Maetz and GarciaRomeu, 1964) presented experimental evidence for direct Na + /NH 4 + exchange linkage in freshwater fish. Since then, our understanding of how ammonia actually permeates the gills has become less and less clear, as various studies have led to conflicting conclusions. Evidence has been presented to reinforce the predominance of Na + /NH 4 + exchange (Maetz, 1973; Kerstetter and Keeler, 1976;Payan and Girard, 1978;Pressley et al., 1981;McDonald and Prior, 1988;McDonald and Milligan, 1988), whereas others have argued for the dominance of simple NH 3 diffusion down the partial pressure NH 3 gradient maintained by the CO 2 hydration reaction in the gill boundary layer (Cameron and Heisler, 1983;Wilson et al., 1994;Wilkie and Wood, 1994). Intermediate positions have included flexible coupling via diffusion trapping of NH 3 linked to Na + /H + or H + pump/Na + channel mechanisms (Avella and Bornancin, 1989;Heisler, 1990), or mixed mechanisms whereby ammonia moves partly by diffusion and partly by electroneutral exchange (Wright and Wood, 1985;Salama et al., 1999). The overall problem is that ammonia excretion h...
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