Page 394 - The Toxicology of Fishes

374 The Toxicology of Fishes

Nucleus and Mitochondria
The formation of binucleated hepatocytes was observed in livers of Epinephelus coioides at one week
after oral exposure to BaP (12.5 µg/g BaP) and the frequency of occurrence increased with the exposure
time. A dose–response relationship was demonstrated between the numerical density of mitochondria
and BaP exposure (up to 5 mg/kg BaP) in Solea ovata (Au et al., 1999, 2004); the higher abundance of
mitochondria after BaP treatments was thought to indicate active cellular metabolism to meet an increased
high demand for ATP. The depletion of glycogen content was observed in a majority of hepatocytes
upon exposure to BaP, regardless of the fish species and the route of exposure (Au et al., 1999, 2004).
Glycogen depletion is a nonspecific adaptive response of hepatocytes to a large variety of xenobiotics
and is generally regarded as a parameter for indicating acute or short-term stress (Arnold et al., 1995;
Biagianti-Risbourg and Bastide, 1995; Braunbeck and Volk, 1991; Eurell and Haensly, 1981; Gluth and
Hanke, 1985; Rojik et al., 1983). Lipid storage in fish liver can be both decreased and increased under
toxicant exposure. Oral administration of 0.5 µg endosulfan per kg food to juvenile carp reduced the
volumetric content of hepatic lipid from 14% to 5%, which may represent a general stress response as
individual hepatocyte volume was also reduced by 50% (Braunbeck and Appelbaum, 1998). In both
male and female zebrafish, exposure to lindane induced a pronounced steatosis microvesicular fatty
transformation of the rough ER cisternae (Braunbeck et al., 1990a). Induction of steatosis by toxicants
has been also reported from mammalian liver, and the underlying mechanism may be the blockage of
lipoprotein secretion from the rough ER and Golgi system (Baglio and Farber, 1965).

Liver Alterations in Fish Exposed to Environmental Pollutants

The relationships between histopathologic lesions in fish livers and exposure to persistent environmental
contaminants were thoroughly studied in large-scale surveys conducted by the U.S. National Marine
Fisheries Services (NMFS). A total of 18 marine bottom fish species collected from 45 sites on the
Pacific coast (Malins et al., 1988; Myers et al., 1993; Varanasi et al., 1989) and 22 sites on the Northeast
coast (Johnson et al., 1992a,b) were included in the surveys. Results demonstrated that megalocytic
hepatosis (MH), foci of cellular alteration (FCA), and biliary and hepatocellular neoplasms were prevalent
in the English sole and other bottom fish species (e.g., rock sole, starry flounder, Pacific staghorn sculpin,
Dover sole, and white croaker), and their prevalences were closely associated with exposure to PAHs,
PCBs, and DDT in sediment, stomach content, and liver (Myers and Rhodes, 1988; Myers et al., 1993).
Similar extensive surveys have also been carried out in Canada, Europe, and Australia to assess the
impact of environmental contaminants on fish health (Au, 2004).
These survey data generally show a good correlation between the concentrations of various persistent
chlorinated hydrocarbons and metals and liver lesions (Köhler, 1990; Malins et al., 1988; Myers et al.,
1992). A recent study by Stehr et al. (2004) in Vancouver Harbour in Canada also demonstrated that the
occurrence of toxicopathic liver lesions in English sole was statistically associated with concentrations
of aromatic hydrocarbon (AH) metabolites in the sediment and AH metabolite levels measured in bile.
Also, in numerous studies on freshwater environments, good correlations between water quality and
liver histopathology have been demonstrated (Handy et al., 2002; Schmidt-Posthaus et al., 2001; Schwai-
ger et al., 1997; Teh 1997). Evidently, fish livers are highly sensitive to pollutant exposure. Fish liver
histopathology is indicative of the general health condition of fish and levels of toxic xenobiotics,
carcinogens, and urban pollution.
Other histopathologic responses, such as escalated macrophage immigration and subsequent increases
in the number of macrophage aggregates (MAs), were observed in the livers of English sole and winter
flounder with liver neoplasms (Myers et al., 1987) as well as in the livers of fish inhabiting degraded
environments (Murchelano and Wolke, 1991). The use of hepatic MA hyperplasia was recommended as
an indicator of health of grey mullet juveniles in contaminated coastal environments (Biagianti-Risbourg,
1993). Fish exposed to pulp mill effluent also showed considerably greater MA in the spleen of winter
flounder (Khan and Payne, 1997) and in the livers of common jollytail and Tasmanian blennies (Wood-
worth et al., 1998). Moreover, field studies have been supported by controlled laboratory investigations,