Carls and Rice: Oil-exposed Theragra chalcogramma embryos 



35 



Table 8 



Percentage of walleye pollock larvae abnormal at the time of hatch following treatment in water-soluble fractions of Cook Inlet crude 

 oil. ANOVA indicates significance of abnormalities by analysis of variance; arc sine transformations were used with proportional data. 

 ***P<0.005, t significant differences from control (Dunnette test. 95% confidence), and +95% confidence. 



7-21 day treatment 



ppm 



% abnormal 



0.00 

 0.26 

 0.68 

 1.83 

 2.80 

 3.14 



6.4 



8.6 



6.6 



16.4 



91.8 



90.9 



± 5.1 



± 13.4 



± 23.2 



± 10.7 



± 12.4 1 

 ± 9.2t 



example, metabolic rates were elevated when larval 

 Pacific herring Clupea harengus pallasi and northern 

 anchovy Engraulis mordax were exposed to benzene 

 (Struhsaker et al. 1974). 



Decreases in larval size and yolk reserves caused by 

 sublethal exposure of developing fish eggs to WSF 

 potentially reduces survival potential. Predator avoid- 

 ance capability tends to increase exponentially with 

 larval length; however, decreases in avoidance behavior 

 may be important only when the difference in size 

 between predator and prey is small (Hunter 1981). Lar- 

 vae with smaller yolk reserves generally have less time 

 to begin feeding before onset of irreversible starvation 

 (Blaxter and Hempel 1963). 



The abnormalities observed in this study are the 

 same, or similar, to those observed in other studies with 

 a variety of species (Rosenthal and Alderdice 1976; 

 Linden 1976; Kiihnhold 1974, 1977) and support the 

 observation by Rosenthal and Alderdice (1976) that fish 

 embryos tend to respond developmentally in similar 

 ways to external stress. Some of the developmental ab- 

 normalities (vesicle formation, body curvatures, and 

 bloated yolks) caused by exposure of pollock eggs to 

 WSF in this experiment were also caused by elevated 

 temperatures in a pollock egg study by K. Krieger and 

 L. Sonenberg (Auke Bay Lab., Alaska Fish. Sci. Cent., 

 Natl. Mar. Fish. Serv., NOAA, P.O. Box 210155, Auke 

 Bay, AK 99821, pers. commun. May 1988). Cold 

 temperatures may cause similar problems in herring 

 larvae: abnormal optic vesicles, enlarged pericardial 

 areas, and jaw abnormalities (Ojaveer 1981). Lighter 

 pigmentation in exposed cod Gadus morhua embryos 

 has been observed in studies involving hydroxylated 

 aromatic hydrocarbons (Falk-Petersen et al. 1985). 



Ion imbalance due to changes in membrane osmo- 

 regulation (Ernst and Neff 1977, Linden 1978) provides 

 a good explanation for yolksac and pericardial defor- 

 mities, because yolksac volumes are related to water 



content (Rosenthal and Alderdice 1976). Aromatic 

 hydrocarbons alter the surface properties of cell mem- 

 branes, possibly modifying their permeability (Roubal 

 and Collier 1975, Aronovich et al. 1975). Structural 

 changes in cell and mitochondrial membranes of larval 

 mummichogs Fundulus heteroclitus exposed to the 

 WSF of Prudhoe Bay crude oil occurred even in larvae 

 which did not show visible abnormalities (Cameron and 

 Smith 1980). 



Previous cell damage, rather than the continued 

 presence of sequestered hydrocarbons, is most likely 

 responsible for the development of abnormalities after 

 hatch, because newly hatched larvae were transferred 

 to clean water and most of the hydrocarbon depurated 

 rapidly (59-83% in the first 8 hours; Carls and Rice 

 1988). In another study, cod larvae also depurated 

 naphthalene quickly, but heavier organic compounds 

 (phenanthrene, benzo(a)pyrene, and 2, 4, 5,2', 4', 5'- 

 hexachlorobiphenyl) were depurated progressively 

 more slowly as molecular weights increased (Solbak- 

 ken et al. 1984). In our study, however, compounds 

 with molecular weights greater than the methylnaph- 

 thalenes were present only at extremely low concen- 

 trations, if at all. An indication that the damage hap- 

 pened early in development, but was expressed later 

 as malformations, was the occurrence of abnormal 

 membranous vesicles 6-9 days after fertilization. At 

 hatch, other malformations were observed which could 

 have been the result of the same or similar mechanisms 

 responsible for vesicle formation, and correlation 

 between early and later abnormalities was very high 

 (r=0.99). 



The significant mortality of larvae exposed to WSF 

 during egg development was probably caused by 

 biochemical changes, structural malformations, or 

 disruption of tissue and organ development rather than 

 a continued presence of hydrocarbons or insufficient 

 yolk reserves. Larval mortality did not exceed 2% 



