Abstract

Juvenile rainbow trout were fed semi-purified diets with (58 μg As/g diet) or without arsenic, added as disodium arsenate heptahydrate (DSA), under standard laboratory conditions for up to 12 weeks, to determine the time-course of development of gallbldder pathology in response to dietary DSA exposure, to correlate this pathology with levels of total arsenic and specific metabolites in the hepatobiliary system and thereby to attempt to gain some insight regarding the mechanism(s) by which the pathological changes develop. Gallbladder lesions associated with this level of dietary arsenic exposure to juvenile rainbow trout include acute inflammation with oedema of the submucosal tissues and sloughing of the epithelium within the first day of exposure, developing to chronic inflammation with fibrosis of the gallbladder wall. These changes may result from the toxic influence of arsenate absorbed into the epithelial cells. The arsenic content of washed gallbladder tissue is a sensitive indicator of recent dietary DSA exposure, while the chronic inflammatory lesion with extensive fibrosis of the gallbladder wall may provide a longer-term indicator of exposure to toxic levels of DSA in the diet of rainbow trout.

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