Fish Gill Structural Changes Induced by Toxicants and Other Irritants: A Statistical Review

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Abstract
Here I quantitatively review the literature on how fish gill morphology is affected by chemical and physical irritants in the surrounding water (e.g. various toxicants, extremes of temperature or pH). I catalogued histopathological gill lesions that were reported, and used statistics to explore how such lesions relate to the irritant-exposure conditions under which they occurred (specifically, to dose and class of irritant, to temperature, and to salinity of the surrounding water). Frequently recorded histopathologic lesions include changes in gill epithelium (lifting, necrosis, hyperplasia, hypertrophy, rupture), bulbing or fusing of gill lamellae, hypersecretion and proliferation of mucocytes, and changes in chloride cells and gill vasculature. I conclude that these lesions are largely nonspecific in nature, as each was detected under many different exposure conditions. The lesions are not entirely independent of exposure conditions, however, as my statistical analysis discerns these trends: (1) Most gill lesion types have been reported more frequently after lethal than after sublethal exposure to irritants. (2) Some lesions were more frequently detected in studies employing heavy metals than in studies using organic toxicants or other irritants; such lesions include necrosis and hypertrophy of gill epithelial cells, plus mucous hypersecretion. (3) Lifting of the branchial epithelium, the most commonly reported lesion, was reported more often in freshwater than in marine fish, suggesting that osmolarity of the ambient water influences this lesion. Little relation was found between recorded lesion frequencies and temperature. Following my statistical analysis, the etiology of irritant-induced gill lesions is considered. The nonspecificity of branchial alterations suggests that they primarily represent stereotyped physiological reactions of gills to stress, and many of them are logically considered defense responses. Some branchial alterations have been considered inflammatory, but I conclude that the literature cannot support that hypothesis. Ultrastructural studies have detected irritant-induced disruptions of branchial epithelial cells, including cytoplasmic vacuolization, autophagosomes and inclusions, loss of microvilli, and abnormal mitochondria and nuclei.