7. Role of Lipids in Fish Populations
147
protein, or glycogen dynamics within the body. If the stress is of sufficient magnitude or duration, then tertiary changes may also be manifested as alterations in
growth, reproduction, or even survival of individuals and populations (Adams,
1990; Wedemeyer et aI., 1984) (Fig. 7.2).
Environmental stressors such as contaminants and unfavorable temperature
regimes are known to alter both the quantity and quality of lipids in fish. Studies
of lipids as an energy source in fish have revealed their importance during periods
of stress (Jezierska et aI., 1982). Stress responses are energy-draining processes
that use triglycerides as the main energy source, although phospholipids may also
be used under severe conditions (Benton et aI., 1994). Energy supplied to the
organism by breakdown of lipids during such increased metabolic demand comes
primarily from oxidation of fatty acids. The free fatty acids yield additional
energy for mitigating or ameliorating the stress condition caused by the impact of
contaminants or other environmental stressors (Tulasi et aI., 1992). Thus, stressors
can deplete the lipid reserves over time, resulting in changes to important physiological processes in the organism.
7.2.4.1. Contaminant Effects
Both increases and decreases in total lipids and triglycerides have been observed
when fish are exposed to contaminants such as pesticides, heavy metals, and
PCBs. A number of studies, mostly involving laboratory exposures, have reported
on the effects of pesticides on lipid levels in the liver and muscle tissue of various
fish species. Benton et al. (1994) observed that the sailfin molly, Poecilia latipinna, exposed to DDT for 21 d demonstrated decreases in total body lipids and
triglycerides that were attributed to increased metabolism (catabolism) following
DDT exposure. Conversely, in juvenile coho and chinook salmon fed DDT in
their diets, carcass lipid content increased (Buhler et aI., 1969). A decrease in liver
lipids was observed in the freshwater fish, Channa punctata, exposed to increasing concentrations of the organochlorine insecticide endosulfan for 96 h (Murty
and Devi, 1982). Exposure of the freshwater catfish, Clarias batrachus, to sublethal concentrations of the pesticide malathion for 4 weeks during the vitellogenic phase of its reproductive cycle resulted in elevated liver lipids (LaL and
Singh, 1987). In this case, elevated liver lipids may have been caused by the
pesticide stimulating lipogenic activity in the liver and increasing fatty acid synthesis. Lipid increases may have also occurred because oxidation and utilization
of fatty acids were inhibited. In female catfish, however, malathion inhibited
mobilization of hepatic phospholipids and free fatty acids to the gonads. Because
the teleostean ovary imports lipids and phospholipids from the liver during the
vitellogenic phase under the influence of sex steroids and gonadotrophin, the
inability of the exposed fish to mobilize these lipids to the gonads may have been
caused by the pesticide reducing circulating levels of sex steroids and gonadotrophins. Freeman and Idler (1975) also reported that organochlorine and organophosphorus compounds suppressed gonadal growth by this mechanism, and Rao
and Rao (1984) found that organophosphorus insecticides inhibited the synthesis
and metabolism of steroid compounds. When tilapia were exposed to the pesticide
147
protein, or glycogen dynamics within the body. If the stress is of sufficient magnitude or duration, then tertiary changes may also be manifested as alterations in
growth, reproduction, or even survival of individuals and populations (Adams,
1990; Wedemeyer et aI., 1984) (Fig. 7.2).
Environmental stressors such as contaminants and unfavorable temperature
regimes are known to alter both the quantity and quality of lipids in fish. Studies
of lipids as an energy source in fish have revealed their importance during periods
of stress (Jezierska et aI., 1982). Stress responses are energy-draining processes
that use triglycerides as the main energy source, although phospholipids may also
be used under severe conditions (Benton et aI., 1994). Energy supplied to the
organism by breakdown of lipids during such increased metabolic demand comes
primarily from oxidation of fatty acids. The free fatty acids yield additional
energy for mitigating or ameliorating the stress condition caused by the impact of
contaminants or other environmental stressors (Tulasi et aI., 1992). Thus, stressors
can deplete the lipid reserves over time, resulting in changes to important physiological processes in the organism.
7.2.4.1. Contaminant Effects
Both increases and decreases in total lipids and triglycerides have been observed
when fish are exposed to contaminants such as pesticides, heavy metals, and
PCBs. A number of studies, mostly involving laboratory exposures, have reported
on the effects of pesticides on lipid levels in the liver and muscle tissue of various
fish species. Benton et al. (1994) observed that the sailfin molly, Poecilia latipinna, exposed to DDT for 21 d demonstrated decreases in total body lipids and
triglycerides that were attributed to increased metabolism (catabolism) following
DDT exposure. Conversely, in juvenile coho and chinook salmon fed DDT in
their diets, carcass lipid content increased (Buhler et aI., 1969). A decrease in liver
lipids was observed in the freshwater fish, Channa punctata, exposed to increasing concentrations of the organochlorine insecticide endosulfan for 96 h (Murty
and Devi, 1982). Exposure of the freshwater catfish, Clarias batrachus, to sublethal concentrations of the pesticide malathion for 4 weeks during the vitellogenic phase of its reproductive cycle resulted in elevated liver lipids (LaL and
Singh, 1987). In this case, elevated liver lipids may have been caused by the
pesticide stimulating lipogenic activity in the liver and increasing fatty acid synthesis. Lipid increases may have also occurred because oxidation and utilization
of fatty acids were inhibited. In female catfish, however, malathion inhibited
mobilization of hepatic phospholipids and free fatty acids to the gonads. Because
the teleostean ovary imports lipids and phospholipids from the liver during the
vitellogenic phase under the influence of sex steroids and gonadotrophin, the
inability of the exposed fish to mobilize these lipids to the gonads may have been
caused by the pesticide reducing circulating levels of sex steroids and gonadotrophins. Freeman and Idler (1975) also reported that organochlorine and organophosphorus compounds suppressed gonadal growth by this mechanism, and Rao
and Rao (1984) found that organophosphorus insecticides inhibited the synthesis
and metabolism of steroid compounds. When tilapia were exposed to the pesticide