Page 52 - The Toxicology of Fishes

32 The Toxicology of Fishes

External
Other Cations Membrane

+2 +2 +?
Cu Cu X Cell Cu
Bulk Water Gill Water

Advection, Toxicity
Diffusion Receptor

CuL CuL X CuL
Bulk Water Gill Water Cell

Bulk Gill
Exposure Water Microenvironment Organism
FIGURE 2.11 Conceptual model for chemical interactions regulating copper bioavailability at fish gills. See text for
explanation of symbols.

the total pool of copper within the gill microenvironment. The various speciation reactions will result
in a distribution of copper species within the gill microenvironment different from that in the bulk
exposure water. These reactions are not necessarily at equilibrium, so bioavailability also can be a
function of the kinetics of these reactions.
Some of these species will interact with or cross the external surface of the gill by various mechanisms
denoted by the ovals marked with an X in Figure 2.11. The extent to which copper is absorbed by the
fish and reaches internal toxicity receptors is represented by the horizontal arrows penetrating the surface.
These arrows are of different thicknesses to denote that the gill surface is often less permeable, but not
necessarily completely impermeable, to copper bound to ligands. Other cations, such as calcium, hydro-
gen, and sodium, might exert an effect on copper bioavailability by competing with copper for sites on
the gill surface, or otherwise affecting the permeability of the gill surface to copper. The arrows again
converge on the other side of the membrane to indicate that any copper entering the organism contributes
to the total pool of copper within cells. This pool of copper is further affected by various speciation
reactions (including changes in copper oxidation state) and is transported to where the different chemical
species can interact with toxicity receptors.
Many of the processes and concepts depicted in Figure 2.11 have been the basis for metal bioavailability
models proposed by various authors. These include model equations presented by Zitko (1976), the gill
surface interaction model described and evaluated by Pagenkopf (1983), the free ion activity model
(FIAM) described by Morel (1983), further developments of the FIAM by Brown and Markich (2000),
and more recently the biotic ligand model, so named because biochemical sites such as those marked
with an X in Figure 2.11 are viewed as other ligands that the metal interacts with (DiToro et al., 2001;
Meyer et al., 1999; Santore et al., 2001). Reviews and critiques of these models are available from
Campbell (1995) and Paquin et al. (2002a).
These models have similar basic features. Toxicity is a function of the amount of metal bound to a
site on the organism surface. This is not necessarily a site of toxic action but rather might be an uptake
site that defines how much metal gets to the toxicity receptors. This site is of central importance to
bioavailability because its external location allows interaction with the exposure water chemistry. The
metal bound at this site is assumed to be in equilibrium with the free metal in the water to which it is
exposed. Complexation by various ligands in the exposure water will therefore limit the amount of metal
binding to the site. Various cations can also bind with the site, creating competitive interactions that also
limit binding of the toxic metal. The models include, or can be readily modified to include, binding of
other species of the toxic metal at the site as mixed ligand complexes, so these species can also contribute
to uptake and toxicity. Of course, it is an oversimplification to depict all relevant effects as arising from
simple chemical mass action of these chemical entities at a single type of site; however, such a
mathematical treatment can still be a useful approximation for the processes that do occur.