Page 35 - The Toxicology of Fishes

Bioavailability of Chemical Contaminants in Aquatic Systems 15

Next Water Channel

T B
B
10 Blood Space
T B
9 Epithelial Tissue
S
7
8
8 1 2 3
6 C Water Channel
T
B
5 4
B T
Next Lamella
FIGURE 2.3 Conceptual model of contaminant uptake at fish gills. Diagram depicts a secondary lamella of a fish gill as
epithelial tissue enclosing a space through which blood flows and shows an adjacent lamellar channel through which water
flows. See text for explanation of symbols.

(dotted arrow 6) and various chemical exchanges at the gill surface (dotted arrows). Changes in this
chemistry can shift the speciation of the toxic chemical, causing net increases or decreases in the amount
of free chemical (arrows 4 and 5, respectively). Chemical characteristics of the exposure water can also
affect uptake rates across the gill epithelium by affecting cellular membrane characteristics (dotted arrows
marked 8); for example, certain chemical constituents might compete with the toxic chemical at, or
otherwise modify the properties of, the exchange site.
After the chemical has been absorbed into and across the epithelium, its speciation can also change.
Toxic chemical that is absorbed while bound to other chemicals will dissociate in the chemical environ-
ment of the organism (forked arrow marked 9), unless the dissociation reaction rate is slow or the same
binding agent exists at similar concentrations within the organism. More importantly, the speciation of
the toxic chemical can be affected by a variety of chemical constituents within the organism (arrow 10).
These various reactions will alter chemical gradients and thus affect uptake, just as binding to hemoglobin
helps maintain high uptake rates of oxygen. If these speciation reactions are rapid enough, each chemical
species in the exposure water that is absorbed will contribute to the internal concentrations of all species
and thus to the effective dose, in proportion to the rate at which it is taken up; however, in cases where
speciation reactions are slow, toxic chemical species inside the fish may retain a “memory” of their
identity outside the fish, such that different species may not contribute to toxicity to the same degree as
they do total accumulation.
Various processes identified in Figure 2.3 are reflected in data from McKim et al. (1985), who measured
the uptake of 14 organic chemicals across the gills of large rainbow trout (Oncorhynchus mykiss). For
neutral organic compounds of moderate hydrophobicity (3 < log K < 6), chemical extraction efficiencies
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(i.e., the fraction of chemical removed from water flowing into the gill) were similar to that of oxygen.
Efficiencies were high for these chemicals because, like oxygen: (1) they exist in exposure water almost
entirely as uncomplexed, small, neutral molecules that can readily diffuse into and across the gill
epithelium, and (2) they bind to certain components in the blood, thereby maintaining a strong diffusion
gradient from water to blood. Accumulation rates for these chemicals are primarily limited by the rate
at which water is pumped through the lamellar water channels.
Less efficient uptake occurred for chemicals with either lower (<3) or higher (>6) log K values and
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for those chemicals that were partially ionized. These lower uptake efficiencies can be understood in
terms of chemical speciation and membrane transport properties. For chemicals with log K < 3, uptake
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is slower because these chemicals do not bind as strongly to blood components, which results in the
free chemical concentrations in the blood increasing significantly during passage through the gill, thereby
reducing diffusion gradients. The accumulation rate of such chemicals is primarily limited by the rate
at which blood flows through the secondary lamellae, in contrast to the water-flow-limited chemicals
discussed above. Chemicals with log K > 6 will diffuse less readily across cellular membranes, either
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