54
3. Toxic Effects of Selenium in Fish
response to the stressor, leading to increased respiration and oxygen
consumption, and depletion of stored body lipids (Lemly and Esch 1984).
If the stressor is a chemical contaminant, for example, selenium, a
variety of sublethal tissue and organ responses can occur and increase
energy requirements (Ribelin and Migaki 1975; Hocutt and Stauffer
1980; Rand and Petrocelli 1985; Lemly 1993b). These factors impinge
on warm-water fish at a time when they are forced to be inactive by
cold temperature. They do not respond behaviorally or physiologically
to offset the metabolic effects of the stressor.
The end result of WSS is often death. As water temperature drops,
the continued presence of a metabolic stressor greatly accelerates the
normal seasonal cycle of lipid depletion. Without this source of energy
to draw upon, the limited feeding that takes place is insufficient to
supply adequate nutrition. The lipid content of young bluegill (Lepomis
macrochirus) , for example, does not normally fall below about 10%
(dry weight) during winter. Bluegill experiencing WSS cannot maintain as much stored lipid, and levels may fall below 5%, which is the
threshold for significant mortality in this species (Lemly 1993b).
Increased Selenium Toxicity
As many as one third of young centrarchids exposed to combined dietary and waterborne selenium at concentrations normally tolerated
in warm conditions may die within one month of the onset of WSS
(Lemly 1993b) (Fig. 3.10). The critical point for survival is reached
when body lipid falls to about 5%, which occurs within 30 to 60 days
once water temperature drops below 10"C. Individuals that have sufficient lipid to live for another 60 days with limited feeding will likely
survive indefinitely, but those with inadequate lipid will not. WSS
causes a 5-fold or greater increase in the sensitivity of young centrarchids
to selenium. In warm conditions (25"C), greater than 25 Jlg Se/g in the
diet (dry weight) and greater than 330 Jlg SelL in water are necessary
to cause significant mortality (Cleveland et al. 1993), but only 5 Jlg
Se/g in the diet and 5 Jlg SelL in water can be lethal to fish experiencing WSS (Lemly 1993b).
In North America, centrarchids (family Centrarchidae) appear to be
at high risk of developing WSS, even in habitats where selenium concentrations are only slightly elevated above background levels. In
Belews Lake, for example, residual selenium concentrations of 1 to 4
Jlg Se/g in sediment and 1 Jlg SelL or less in water were sufficient to
cause WSS. The greatest threat is to young-of-the-year and yearling
fish, because they reduce activity and feeding during winter to a greater
extent than older age classes. The population and community-level
implications are serious, because a large percentage (a third or more)
3. Toxic Effects of Selenium in Fish
response to the stressor, leading to increased respiration and oxygen
consumption, and depletion of stored body lipids (Lemly and Esch 1984).
If the stressor is a chemical contaminant, for example, selenium, a
variety of sublethal tissue and organ responses can occur and increase
energy requirements (Ribelin and Migaki 1975; Hocutt and Stauffer
1980; Rand and Petrocelli 1985; Lemly 1993b). These factors impinge
on warm-water fish at a time when they are forced to be inactive by
cold temperature. They do not respond behaviorally or physiologically
to offset the metabolic effects of the stressor.
The end result of WSS is often death. As water temperature drops,
the continued presence of a metabolic stressor greatly accelerates the
normal seasonal cycle of lipid depletion. Without this source of energy
to draw upon, the limited feeding that takes place is insufficient to
supply adequate nutrition. The lipid content of young bluegill (Lepomis
macrochirus) , for example, does not normally fall below about 10%
(dry weight) during winter. Bluegill experiencing WSS cannot maintain as much stored lipid, and levels may fall below 5%, which is the
threshold for significant mortality in this species (Lemly 1993b).
Increased Selenium Toxicity
As many as one third of young centrarchids exposed to combined dietary and waterborne selenium at concentrations normally tolerated
in warm conditions may die within one month of the onset of WSS
(Lemly 1993b) (Fig. 3.10). The critical point for survival is reached
when body lipid falls to about 5%, which occurs within 30 to 60 days
once water temperature drops below 10"C. Individuals that have sufficient lipid to live for another 60 days with limited feeding will likely
survive indefinitely, but those with inadequate lipid will not. WSS
causes a 5-fold or greater increase in the sensitivity of young centrarchids
to selenium. In warm conditions (25"C), greater than 25 Jlg Se/g in the
diet (dry weight) and greater than 330 Jlg SelL in water are necessary
to cause significant mortality (Cleveland et al. 1993), but only 5 Jlg
Se/g in the diet and 5 Jlg SelL in water can be lethal to fish experiencing WSS (Lemly 1993b).
In North America, centrarchids (family Centrarchidae) appear to be
at high risk of developing WSS, even in habitats where selenium concentrations are only slightly elevated above background levels. In
Belews Lake, for example, residual selenium concentrations of 1 to 4
Jlg Se/g in sediment and 1 Jlg SelL or less in water were sufficient to
cause WSS. The greatest threat is to young-of-the-year and yearling
fish, because they reduce activity and feeding during winter to a greater
extent than older age classes. The population and community-level
implications are serious, because a large percentage (a third or more)