90
5. Teratogenic Deformity Index for Fish
larly in the yolk. When the eggs hatch, larval fish rapidly utilize the
selenium-contaminated yolk as both an energy supply and a source of
protein for building new body tissues. Hard and soft tissues may be
deformed if the molecular structure of the protein building blocks has
been distorted due to substitution of selenium for sulfur. Some tissues
may not be generated at all, resulting in missing body parts.
The prevalence of teratogenic deformities increases rapidly once selenium concentrations in eggs exceed 1 0
Se/g (Woock et al. 1987). Hatchability of eggs is not affected by elevated selenium, even though there
may be a high incidence of deformities in resultant larvae and fry, and
many may fail to survive (Gillespie and Baumann 1986; Coyle et al.
1993). The time of induction of teratogenesis is when larval fish are relying on their attached yolk sac for nourishment and development. Once
external feeding begins, the potential for teratogenic effects declines and
soon disappears. Feeding excessive selenium (up to lethal levels) to fry or
juvenile fish as they are growing will not cause teratogenic malformations to occur (Hamilton et al. 1990; Cleveland et al. 1993). Moreover,
dietary selenium levels sufficient to load eggs beyond teratogenic thresholds (a diet including 5-20
Se/g) do not cause teratogenesis in parent
fish or otherwise generally affect their health or survival (Coyle et al.
1993). Thus, the teratogenic process is strictly an egg-larvae phenomenon. Because of this, teratogenesis can be a very subtle, but important,
cause of reproductive failure in fish. Entire populations may disappear
with little evidence of "toxicity", since major impacts to early life stages
can be taking place at the same time that adult fish appear healthy
(Cumbie and Van Horn 1978; Lemly 1985).
Mortality of larval fish can be high if the teratogenic defects are severe
enough to impair critical body functions (Woock et al. 1987). However, in
some cases the abnormalities may not be life threatening, and the malformations can persist into juvenile and adult life stages (Lemly 1993).
This is likely restricted to locations where there is little threat from predators, since all but the most subtle deformities would probably compromise
a fish's ability to feed and avoid predators. Thus, in assessing the prevalence of teratogenic defects, it is important to focus on the earliest life
stages, that is, newly emerging larvae and young fry.
Identifying Teratogenic Deformities
Teratogenic deformities can occur in most, if not all, hard or soft tissues of the body. However, some of the most conspicuous (consequently,
the most diagnostic) are found in the skeleton, fins, head, and mouth.
These typically involve: (1) lordosis, concave curvature of the lumbar
region of the spine; (2) scoliosis, lateral curvature of the spine; (3)
kyphosis, convex curvature of the thoracic region of the spine result-
5. Teratogenic Deformity Index for Fish
larly in the yolk. When the eggs hatch, larval fish rapidly utilize the
selenium-contaminated yolk as both an energy supply and a source of
protein for building new body tissues. Hard and soft tissues may be
deformed if the molecular structure of the protein building blocks has
been distorted due to substitution of selenium for sulfur. Some tissues
may not be generated at all, resulting in missing body parts.
The prevalence of teratogenic deformities increases rapidly once selenium concentrations in eggs exceed 1 0
Se/g (Woock et al. 1987). Hatchability of eggs is not affected by elevated selenium, even though there
may be a high incidence of deformities in resultant larvae and fry, and
many may fail to survive (Gillespie and Baumann 1986; Coyle et al.
1993). The time of induction of teratogenesis is when larval fish are relying on their attached yolk sac for nourishment and development. Once
external feeding begins, the potential for teratogenic effects declines and
soon disappears. Feeding excessive selenium (up to lethal levels) to fry or
juvenile fish as they are growing will not cause teratogenic malformations to occur (Hamilton et al. 1990; Cleveland et al. 1993). Moreover,
dietary selenium levels sufficient to load eggs beyond teratogenic thresholds (a diet including 5-20
Se/g) do not cause teratogenesis in parent
fish or otherwise generally affect their health or survival (Coyle et al.
1993). Thus, the teratogenic process is strictly an egg-larvae phenomenon. Because of this, teratogenesis can be a very subtle, but important,
cause of reproductive failure in fish. Entire populations may disappear
with little evidence of "toxicity", since major impacts to early life stages
can be taking place at the same time that adult fish appear healthy
(Cumbie and Van Horn 1978; Lemly 1985).
Mortality of larval fish can be high if the teratogenic defects are severe
enough to impair critical body functions (Woock et al. 1987). However, in
some cases the abnormalities may not be life threatening, and the malformations can persist into juvenile and adult life stages (Lemly 1993).
This is likely restricted to locations where there is little threat from predators, since all but the most subtle deformities would probably compromise
a fish's ability to feed and avoid predators. Thus, in assessing the prevalence of teratogenic defects, it is important to focus on the earliest life
stages, that is, newly emerging larvae and young fry.
Identifying Teratogenic Deformities
Teratogenic deformities can occur in most, if not all, hard or soft tissues of the body. However, some of the most conspicuous (consequently,
the most diagnostic) are found in the skeleton, fins, head, and mouth.
These typically involve: (1) lordosis, concave curvature of the lumbar
region of the spine; (2) scoliosis, lateral curvature of the spine; (3)
kyphosis, convex curvature of the thoracic region of the spine result-