148
S.M. Adams
methyl parathion for only 48 h, the total lipids and phospholipids decreased in the
muscle and liver, but the free fatty acid levels increased (Rao and Rao, 1984). The
decreased lipid levels indicated glyconeogenesis in these tissues, whereas the
increased free fatty acids along with the decreased tissue lipids suggested increased lipolysis. Increase in fatty acids at the expense of utilization of body lipids
indicated that these compounds were used for extra energy to mitigate the stress
effects of pesticide exposure. Other investigators have also observed fatty livers
following exposure to organochlorine compounds such as PCB (Klaunig et aI.,
1979; Lipsky et aI., 1978). Lipid accumulation in this organ appears to result from
an inability to convert lipids in hepatocytes to a form suitable for use by the
organism (Runnells et aI., 1965).
Lipid stores can serve a protective function from the toxicant effects of contaminants. The herbicide atrazine caused liver lipid degeneration in grey mullet
after a 21-d exposure (Biagianti-Risbourg and Bastide, 1995). Following exposure, the size of lipid droplets increased in the liver. According to Fabacher and
Chambers (1971), lipid droplets can sequester fat-soluble contaminants such as
pesticides and herbicides, providing protection for the organism from the toxic
effects of these chemicals by a dilution effect of the contaminant in the body
tissue. Geyer et ai. (1994) also reported that lipids in aquatic organisms serve as a
protective reservoir against the toxic effects of lipophilic, relatively persistent
organic chemicals because they bioconcentrate mainly in the body lipids. Therefore, in organisms with high lipid content, only a relatively small fraction of
hydrophobic chemicals may actually reach target organs. The disadvantage of this
protective effect, however, is that lipids can bioconcentrate high levels of these
contaminants and may ultimately cause toxicological problems once lipids are
mobilized for the high energy demands of overwinter survival, gonadal development, spawning activities, or migration. In their DDT exposure experiments,
Buhler et ai. (1969) speculated that increases in lipid levels under certain types of
contaminant exposure may represent a compensatory protective response by the
fish to provide additional pesticide storage capacity. Following exposure of mosquitofish in drainage ditches containing insecticides, Fabacher and Chambers
(1971) also concluded that high lipid concentration served as a protective reservoir to the organism against lipophilic contaminants. A disadvantage, however, of
allocating contaminants to lipid stores is that these contaminants are usually
biomagnified through the food chain, increasing the potential toxic effects on
predators and even to human consumers.
Heavy metal exposure also has been found to have variable effects on lipid
dynamics in the organism. Tulasi et ai. (1992) exposed the freshwater fish Anabas
testudinus to sublethal concentrations of lead nitrate for 30 d and found that total
lipids and phospholipids in the ovary and liver decreased while free fatty acids
increased. Lead apparently affects lipid metabolism of fish and may impair fecundity and reduce reproductive success. The effects of mercuric chloride on freshwater catfish exposed to 0.2 mg . L - I for 10, 20, and 30 d were reported by Bano
and Hasan (1989). Total lipid and phospholipid increased in both liver and muscle
tissue, whereas peroxidation of endogenous lipids in these tissues also increased.
S.M. Adams
methyl parathion for only 48 h, the total lipids and phospholipids decreased in the
muscle and liver, but the free fatty acid levels increased (Rao and Rao, 1984). The
decreased lipid levels indicated glyconeogenesis in these tissues, whereas the
increased free fatty acids along with the decreased tissue lipids suggested increased lipolysis. Increase in fatty acids at the expense of utilization of body lipids
indicated that these compounds were used for extra energy to mitigate the stress
effects of pesticide exposure. Other investigators have also observed fatty livers
following exposure to organochlorine compounds such as PCB (Klaunig et aI.,
1979; Lipsky et aI., 1978). Lipid accumulation in this organ appears to result from
an inability to convert lipids in hepatocytes to a form suitable for use by the
organism (Runnells et aI., 1965).
Lipid stores can serve a protective function from the toxicant effects of contaminants. The herbicide atrazine caused liver lipid degeneration in grey mullet
after a 21-d exposure (Biagianti-Risbourg and Bastide, 1995). Following exposure, the size of lipid droplets increased in the liver. According to Fabacher and
Chambers (1971), lipid droplets can sequester fat-soluble contaminants such as
pesticides and herbicides, providing protection for the organism from the toxic
effects of these chemicals by a dilution effect of the contaminant in the body
tissue. Geyer et ai. (1994) also reported that lipids in aquatic organisms serve as a
protective reservoir against the toxic effects of lipophilic, relatively persistent
organic chemicals because they bioconcentrate mainly in the body lipids. Therefore, in organisms with high lipid content, only a relatively small fraction of
hydrophobic chemicals may actually reach target organs. The disadvantage of this
protective effect, however, is that lipids can bioconcentrate high levels of these
contaminants and may ultimately cause toxicological problems once lipids are
mobilized for the high energy demands of overwinter survival, gonadal development, spawning activities, or migration. In their DDT exposure experiments,
Buhler et ai. (1969) speculated that increases in lipid levels under certain types of
contaminant exposure may represent a compensatory protective response by the
fish to provide additional pesticide storage capacity. Following exposure of mosquitofish in drainage ditches containing insecticides, Fabacher and Chambers
(1971) also concluded that high lipid concentration served as a protective reservoir to the organism against lipophilic contaminants. A disadvantage, however, of
allocating contaminants to lipid stores is that these contaminants are usually
biomagnified through the food chain, increasing the potential toxic effects on
predators and even to human consumers.
Heavy metal exposure also has been found to have variable effects on lipid
dynamics in the organism. Tulasi et ai. (1992) exposed the freshwater fish Anabas
testudinus to sublethal concentrations of lead nitrate for 30 d and found that total
lipids and phospholipids in the ovary and liver decreased while free fatty acids
increased. Lead apparently affects lipid metabolism of fish and may impair fecundity and reduce reproductive success. The effects of mercuric chloride on freshwater catfish exposed to 0.2 mg . L - I for 10, 20, and 30 d were reported by Bano
and Hasan (1989). Total lipid and phospholipid increased in both liver and muscle
tissue, whereas peroxidation of endogenous lipids in these tissues also increased.