The fish gill plays a critical role in the maintenance of acid-base and ion balance, as well as gas exchange. The large convection requirement for respiration in water and the extensive areas of exposed membrane on the branchial epithelium, ensure that the gill is also a major site of interaction with waterborne contaminants. This review attempts to summarize the effects of inorganic, organometallic, and organic pollutants on gill physiology, biochemistry, and histopathology. Emphasis is placed on mechanisms of toxicity at environmentally relevant pollutant levels.
The best understood mechanisms of toxicity to the gills are those due to metallic cations. Ionoregulatory failure occurs by chemical-biological interactions with at least two discrete sites: (1) at low external concentrations, ion influx is inhibited; and (2) at higher concentrations, ion efflux is stimulated. The inhibition of influx is due in large part to the binding of metal ions to sulphydryl groups on transport proteins (ATPases), while the stimulation of efflux appears to be governed by the displacement of calcium from the intercellular tight junctions of the epithelial cells. Chloride cell proliferation and ATPase induction are frequently reported results of metal exposure. Ultrastructural changes in tight junctions have also been reported recently. The role of metallothionein or other metal-binding proteins in acclimation is equivocal. Inorganic anions also appear to affect ionoregulation.
There is little information on the effects of organometallics or organics on the gills, when exposed to environmentally relevant concentrations. The gill possesses many of the detoxifying enzymes found in the liver, and there are reports of induction of cytochrome P-450 and uridine diphosphoglucuronosyl transferase in the gills, but with the exception of the carboxylesterases, there is no information on the relevance of these enzymes to bioaccumulation. The gills play a role in the excretion of some organic compounds (log P < 3). There are many reports of pesticides inhibiting ATPases in vitro, as well as some equivocal information that such effects occur in vivo at relevant concentrations. Exposure of caged fish to pulp mill effluents leads to chloride cell hypertrophy and hyperplasia, and plasma ion changes. Since cortisol controls ATPase induction, the proliferation of chloride cells may be part of a general stress response.