Page 861 - The Toxicology of Fishes

Reproductive Impairment of Great Lakes Lake Trout by Dioxin-Like Chemicals 841

Unexposed
A

HYP
H
H
CFM
PE
YSE
DV

TCDD Exposed

B
FIGURE 21.6 Lake trout sac fry unexposed (top) and exposed (bottom) as fertilized eggs to 2,3,7,8-tetrachlorodibenzo-
p-dioxin (TCDD). Sac fry exposed to TCDD have external signs of toxicity, including yolk sac edema (YSE) and pericardial
edema (PE) associated with damage to vascular tissues (DV), hemorrhaging (H), craniofacial malformations (CFM), and
hyperpigmentation (HYP), which lead to death prior to the swim-up stage of development. (From Cook, P.M. et al., Environ.
Sci. Technol., 37, 3867–3877, 2003. With permission.)

has been detected in lake trout embryos prior to hatch (Guiney et al., 1997, 2000). It is significant that
all PCB, PCDD, and PCDF AhR agonists, tested as single compounds or as mixtures, produce identical
signs of early-life-stage toxicity in trout that culminate in mortality from hatching until swim-up. At
higher egg doses, signs of toxicity are invariably manifested earlier during the sac fry stage.

Pathologic Alterations
Spitsbergen et al. (1991) described the pathologic alterations in early life stages of lake trout exposed
as newly fertilized eggs to an LD dose of TCDD (400 pg TCDD per g wet egg). Toxicity was first
100
detected about one week prior to hatch and in larvae that survived hatching toxicity was manifested
during the sac fry stage. The signs of TCDD toxicity in the lake trout sac fry (Figure 21.6) include the
following:
• Retrobulbar, meningeal, subcutaneous, and pericardial petechial hemorrhages
• Severe subcutaneous edema of the yolk sac, with cessation of blood flow in the yolk sac and
body