Page 428 - The Toxicology of Fishes

408 The Toxicology of Fishes

0.6
V (nmol min –1 mg –1 ) 0.4
0.5

0.3
0.2
0.1
0.0
0 10 –12 10 –11 10 –10 10 –9
2+
–1
[Cd ] (mol L )
2+
FIGURE 8.4 Cd inhibition of the ATP-dependent calcium pump in basolateral plasma membrane vesicles from the
intestinal epithelium of Mozambique tilapia (Oreochromis mossambicus). Means ± SEM of nine experiments are given.
2+
2+
The Ca concentration was kept constant at 200 nM. Initial rates of ATP-dependent Ca uptake were corrected for ATP-
independent uptake. The calculated IC 50 is 8.2 ± 3.0 pM Cd . (From Schoenmakers, T. J. M. et al., J. Membr. Biol., 127,
2+
161–172, 1992. With permission.)
activity and possibly also the cotransporter and affected the cation selectivity of the tight junctions.
–
+
Because Na and Cl absorption is the main driving force for intestinal water uptake, these effects of
Cd seriously threaten the water balance of marine fish (Lionetto et al., 1998).
2+
When considering the toxicity of metal ions in a marine environment, it should be kept in mind that
speciation effects, such as the formation of metal chlorides, drastically reduce metal toxicity. For
2+
cadmium, only a very small fraction is present as Cd in seawater. In the intestine, cadmium is readily
bound to the organic material present in this organ. Marked intestinal accumulation of waterborne
cadmium and copper has been reported for freshwater fish (Handy, 1992). Because the low drinking rate
in these animals could not account for this accumulation, the authors suggested a special role for the
intestine as a store and excretion route for these metals, as suggested before for rats (Stonard and Webb,
1976). At high concentrations, cadmium may disrupt the mucosal folds in the intestine, as reported by
Ghosh and Chakrabarti (1992) for Notopterus notopterus. These authors reported that the enterocytes
were losing their regular arrangement and became necrotic, whereas the mucus secretion was stimulated.
Such histopathological changes in fish intestine have also been reported for copper (Bakshi, 1991). In
a study on Atlantic salmon, Lundebye et al. (1998) have shown that dietary copper and cadmium at high
–1
concentrations (up to 700 and 5 mg kg diet, respectively) induced necrosis as well as apoptosis of
enterocytes. Tissue necrosis may be accompanied by enhanced permeability of the epithelium to water
and ions.
Although a direct comparison of exposure to waterborne and dietary heavy metals is complicated,
dietary exposure to copper or cadmium is generally considered less toxic than exposure via the water
(Lanno et al., 1985; Miller et al., 1993). This has been ascribed to the characteristics of the intestinal
epithelium, which apparently represents a more effective and less sensitive barrier to toxic metals than
the branchial epithelium (Handy, 1993). The complexation of metals with the organic contents of the
gut, as mentioned above, may be another mitigating factor.

Organic Pollutants
No studies focusing on the effects of organic pollutants on the hydromineral functions of the fish intestine
are known to the authors. Interference with these functions can only be deduced from the disruptive
effects reported on the structure of the intestinal tracts and from a few studies on intestinal ion-dependent
ATPase activity. Spitsbergen et al. (1988), for example, reported submucosal gastric edema and epithelial
necrosis in perch and rainbow trout treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Such
effects, reported for many organic pollutants, would affect the water and ion balance as a result of
nonspecific damage inflicted to the intestinal epithelium and, more indirectly, via the induction of a
stress response. Chronic stress in fish, as in tetrapods, is known to be accompanied by gastric and
intestinal lesions (Peters, 1982; Szakolczai, 1997).