Page 863 - The Toxicology of Fishes
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Reproductive Impairment of Great Lakes Lake Trout by Dioxin-Like Chemicals  843



                                         Species sensitivity of embryo-larval stages
                                  2500
                                         toward 2,3,7,8-tetrachlorodibenzo-p-dioxin

                                 2,3,7,8-TCDD LD50 (pg/g-egg)  1500
                                  2000






                                  1000


                                   500



                                    0
                                                      Fathead minnow
                                                                          White sucker
                                                                 Lake herring
                                             Rainbow trout
                                      Lake trout Brook trout Fundulus heteroclitus  Channel catfish  Medaka  Northern pike Zebrafish


                       FIGURE 21.7 Species sensitivity towards 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Embryos were exposed as freshly
                       fertilized eggs by waterbath during water hardening or egg injection prior to epiboli. (Data are from Elonen et al., 1998;
                       Guiney et al., 1996, 1997; Helder, 1981; Henry et al., 1997; Toomey et al., 2001; Walker and Peterson, 1994b; Walker et
                       al., 1991; Wright, 2006.)


                       vascular endothelium by TCDD may trigger  edema and vascular dysfunction between hatching and
                       swim-up; that is, a cascade of events initiated by AhR binding of TCDD may increase the permeability
                       of vascular endothelial cells culminating in edema. In support of this interpretation, Guiney et al. (1998)
                       showed that yolk sac edema fluid in TCDD-exposed lake trout is an ultrafiltrate of blood. What is not
                       known is whether induction of CYP1A catalytic activity or some other event subsequent to AhR activation
                       by  TCDD in the vascular endothelium of lake trout sac fry is causally related to  TCDD-induced
                       cardiovascular dysfunction. Evidence from zebrafish indicates that induction of CYP1A in the endothelial
                       cells or other locations of the developing fish embryo is not required for developmental effects of AhR-
                       related toxicity (Carney et al., 2004); however, these same finding have not been demonstrated in trout,
                       particularly lake trout. Although it is highly likely that the mechanistic findings related to the toxicity
                       of AhR ligands observed in zebrafish are applicable to salmonine species, some verification of this model
                       is needed.



                       Species Differences in TCDD Toxic Potency
                       The susceptibility of freshwater fish species to early-life-stage mortality caused by exposure of fertilized
                       eggs to TCDD varies widely. The rank order sensitivity for 11 fish species shows that lake trout is the
                       most sensitive, followed by brook trout and rainbow trout (Figure 21.7). The eight non-salmonine species
                       are less sensitive. The rank order, beginning with the most sensitive fish species (based on egg TCDD
                       LD ), is lake trout (40 to 85 pg/g), brook trout (138 to 200 pg/g), rainbow trout (230 to 488 pg/g),
                         50
                       Atlantic killifish (Fundulus heteroclitus) (250 pg/g), fathead minnow (539 pg/g), channel catfish (644
                       pg/g), lake herring (902 pg/g), medaka (1110 pg/g), white sucker (1890 pg/g), northern pike (2460 pg/g),
                       and zebrafish (2610 pg/g) (Elonen et al., 1998; Guiney et al., 1996, 1997; Helder, 1981; Henry et al.,
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