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HISTOPATHOLOGICAL EVIDENCE OF REGENERATION FOLLOWING HEPATOTOXIC EFFECTS OF THE CYANOTOXIN MICROCYSTIN-LR IN THE HARDHEAD CATFISH AND GULF KILLIFISH.
Citation:
Fournie, J W. AND L A. Courtney. HISTOPATHOLOGICAL EVIDENCE OF REGENERATION FOLLOWING HEPATOTOXIC EFFECTS OF THE CYANOTOXIN MICROCYSTIN-LR IN THE HARDHEAD CATFISH AND GULF KILLIFISH. JOURNAL OF AQUATIC ANIMAL HEALTH 14(4):273-280, (2002).
Description:
The cyanobacterial toxin, microcystin-LR (MC-LR), causes liver damage in several freshwater fish species. The damage appears to be acute and irreversible. In the present study, two estuarine species, hardhead catfish, Arius felis, and gulf killifish, Fundulus grandis, were injected intraperitoneally with MC-LR and livers examined histopathologically for up to 23 d post injection (PI) in catfish and 5 d PI in killifish. Livers from both species exhibited extensive, diffuse hepatocellular necrosis by 6 h PI. By day 2, the necrosis persisted and large numbers of basophilic cells emerged throughout the liver parenchyma. The basophilic cells occurred
individually or in small clusters. By 72 h, the basophilic cells appeared highly proliferative with numerous mitotic figures and were arranged in cords and tubules similar to mature hepatic parenchyma. Regeneration of the liver parenchyma was noted in gulf killifish at 5 d PI as tracts of basophilic cells were still evident. In hardhead catfish, there were no signs of necrosis or proliferating basophilic cells by 9 d PI and the hepatic parenchyma appeared normal except for vacuolation of many hepatocytes and some areas of hepatic megalocytosis. Degenerative changes in the hardhead catfish and gulf killifish were similar to those observed in freshwater fish species exposed to MC-LR but were more pronounced in the marine species. Evidence of
recovery from the hepatotoxic effects of MC-LR suggest the toxin might be used to study regenerative processes in fish liver.