Identifying Teratogenic Deformities
91
ing in "humpback" condition; (4) missing or deformed fins; (5) missing or deformed gills or gill covers (opercle); (6) abnormally shaped
head; (7) missing or deformed eyes; (8) deformed mouth. (See Figs.
3.5-3.9, Chapter 3, for a description of deformities.)
In general, a careful fish-in-hand inspection is sufficient to diagnose
any of the major teratogenic deformities. However, to make the diagnosis
for larvae and fry or small species (eg, small cyprinids, poeciliids), or in
situations when it is necessary to tabulate all of the subtle, less overt
symptoms (eg, slightly deformed fins, opercles, etc.) the fish must be carefully examinated with the aid of a dissection microscope. This is particularly true for larval fish. Some of their undeveloped features could
erroneously be considered a defect, when in fact, they are a consequence
of a premature life stage, not selenium teratogenesis. However, this is not
a serious concern because larval fish have distinctive patterns of development that quickly become apparent to the investigator looking for teratogenesis. With a bit of hands-on experience, the true teratogenic defects
are easily distinguishable even in young fish (see Fig. 3.5, Chapter 3).
There are some other symptoms of selenium poisoning that may be
confused with teratogenic effects. These are generally thought to represent acute toxic responses to high doses or tissue concentrations of
selenium rather than true teratogenic effects. The most common of
these symptoms are: (1) edema, swollen and distended abdomen due
to accumulation of fluid in the visceral cavity; (2) exopthalmus (bulging or protruding eyes) due to accumulation of fluid in the eye sockets;
and (3) cataracts, which appear as a white coating on the eyes (see
Figs. 3.3-3.5, Chapter 3). All of these symptoms may be present concurrently, along with the true teratogenic effects. Particular care must
be exercised when examining larval fish. Edematous larvae with distended abdomens are common (eg, Bryson et al. 1984; Gillespie and
Baumann 1986; Pyron and Beitinger 1989). This condition may progress
to, or be associated with, the expression of terata, but the edema itself
does not constitute a teratogenic defect. However, severe edema is
usually accompanied by deformity of the spine (most often lordosis) or
soft tissues in the abdomen. The prevalence of edema and terata can
be virtually the same (eg, Schultz and Hermanutz 1990) or quite different (eg, Hermanutz et al. 1992). Thus, one should not assume a 1:1
relationship. Reasonable caution, that is, close inspection and comparison with normal larvae, will prevent inaccurate diagnoses.
In order to draw a conclusion of selenium-induced teratogenesis,
the visual indicators and symptoms (deformities) must be corroborated
with the presence of elevated concentrations of selenium in tissues.
Concentrations in the range of 10 to 20 Ilg Se/g or greater (whole-body
homogenate) would be sufficient to confirm the diagnosis. This corresponds to concentrations of about 6 to 12 Ilg Se/g in muscle (fillets) or
20 to 40 Ilg Se/g in visceral tissues, including the liver. Although mea-
91
ing in "humpback" condition; (4) missing or deformed fins; (5) missing or deformed gills or gill covers (opercle); (6) abnormally shaped
head; (7) missing or deformed eyes; (8) deformed mouth. (See Figs.
3.5-3.9, Chapter 3, for a description of deformities.)
In general, a careful fish-in-hand inspection is sufficient to diagnose
any of the major teratogenic deformities. However, to make the diagnosis
for larvae and fry or small species (eg, small cyprinids, poeciliids), or in
situations when it is necessary to tabulate all of the subtle, less overt
symptoms (eg, slightly deformed fins, opercles, etc.) the fish must be carefully examinated with the aid of a dissection microscope. This is particularly true for larval fish. Some of their undeveloped features could
erroneously be considered a defect, when in fact, they are a consequence
of a premature life stage, not selenium teratogenesis. However, this is not
a serious concern because larval fish have distinctive patterns of development that quickly become apparent to the investigator looking for teratogenesis. With a bit of hands-on experience, the true teratogenic defects
are easily distinguishable even in young fish (see Fig. 3.5, Chapter 3).
There are some other symptoms of selenium poisoning that may be
confused with teratogenic effects. These are generally thought to represent acute toxic responses to high doses or tissue concentrations of
selenium rather than true teratogenic effects. The most common of
these symptoms are: (1) edema, swollen and distended abdomen due
to accumulation of fluid in the visceral cavity; (2) exopthalmus (bulging or protruding eyes) due to accumulation of fluid in the eye sockets;
and (3) cataracts, which appear as a white coating on the eyes (see
Figs. 3.3-3.5, Chapter 3). All of these symptoms may be present concurrently, along with the true teratogenic effects. Particular care must
be exercised when examining larval fish. Edematous larvae with distended abdomens are common (eg, Bryson et al. 1984; Gillespie and
Baumann 1986; Pyron and Beitinger 1989). This condition may progress
to, or be associated with, the expression of terata, but the edema itself
does not constitute a teratogenic defect. However, severe edema is
usually accompanied by deformity of the spine (most often lordosis) or
soft tissues in the abdomen. The prevalence of edema and terata can
be virtually the same (eg, Schultz and Hermanutz 1990) or quite different (eg, Hermanutz et al. 1992). Thus, one should not assume a 1:1
relationship. Reasonable caution, that is, close inspection and comparison with normal larvae, will prevent inaccurate diagnoses.
In order to draw a conclusion of selenium-induced teratogenesis,
the visual indicators and symptoms (deformities) must be corroborated
with the presence of elevated concentrations of selenium in tissues.
Concentrations in the range of 10 to 20 Ilg Se/g or greater (whole-body
homogenate) would be sufficient to confirm the diagnosis. This corresponds to concentrations of about 6 to 12 Ilg Se/g in muscle (fillets) or
20 to 40 Ilg Se/g in visceral tissues, including the liver. Although mea-