Pink Salmon Embryos Research Articles

Exposure of pink salmon embryos to dissolved polynuclear aromatic hydrocarbons delays development, prolonging vulnerability to mechanical damage

Exposure to dissolved polynuclear aromatic hydrocarbons (PAHs) from crude oil delays pink salmon (Oncorhynchus gorbuscha) embryo development, thus prolonging their susceptibility to mechanical damage (shock). Exposure also caused mortality, edema, and anemia consistent with previous studies. Hatching and yolk consumption were delayed, indicating the rate of embryonic development was slowed by PAH exposure. The net result was that exposed embryos were more susceptible to shock than normal, unexposed embryos. Susceptibility to shock was protracted by 4-6d for more than a month in embryos exposed to exponentially declining, dissolved PAH concentrations in water passed through oiled rock; the initial total PAH concentration was 22.4microgL(-1) and the geometric mean concentration was 4.5microgL(-1) over the first 20d. Protracted susceptibility to shock caused by exposure to PAHs dissolved from oil could potentially increase the reported incidence of mortality in oiled stream systems, such as those in Prince William Sound after the Exxon Valdez oil spill, if observers fail to discriminate between direct mortality and shock-induced mortality.

Risk of weathered residual Exxon Valdez oil to pink salmon embryos in Prince William Sound

It has been hypothesized that pink salmon eggs incubating in intertidal streams transecting Prince William Sound (PWS) beaches oiled by the Exxon Valdez oil spill were exposed to lethal doses of dissolved hydrocarbons. Since polycyclic aromatic hydrocarbon (PAH) levels in the incubation gravel were too low to cause mortality, the allegation is that dissolved high-molecular-weight hydrocarbons (HPAH) leaching from oil deposits on the beach adjacent to the streams were the source of toxicity. To evaluate this hypothesis, we placed pink salmon eggs in PWS beach sediments containing residual oil from the Exxon Valdez oil spill and in control areas without oil. We quantified the hydrocarbon concentrations in the eggs after three weeks of incubation. Tissue PAH concentrations of eggs in oiled sediments were generally < 100 ppb and similar to background levels on nonoiled beaches. Even eggs in direct contact with oil in the sediment resulted in tissue PAH loads well below the lethal threshold concentrations established in laboratory bioassays, and very low concentrations of HPAH compounds were present. These results indicate that petroleum hydrocarbons dissolved from oil deposits on intertidal beaches are not at concentrations that pose toxic risk to incubating pink salmon eggs. The evidence does not support the hypothesis that interstitial pore water in previously oiled beaches is highly toxic.

Comment on "Toxicity of Weathered Exxon Valdez Crude Oil to Pink Salmon Embryos."

Comment on "Toxicity of Weathered Exxon Valdez Crude Oil to Pink Salmon Embryos."

Toxicity of weathered Exxon Valdez crude oil to pink salmon embryos

Research was conducted at the University of Idaho (Moscow, ID, USA) on the toxicity of weathered Exxon Valdez crude oil to embryos of pink salmon from 2001 to 2003 for the purpose of comparing these data with those from the National Oceanic and Atmospheric Administration Fisheries Laboratory at Auke Bay (AK, USA). Mortality reported at Auke Bay for embryos chronically exposed to very low concentrations of aqueous solutions of weathered oil, measured as dissolved polycyclic aromatic hydrocarbons (PAHs), was inconsistent with that in other published research. Using the Auke Bay experimental design, we found that toxicity is not evident in pink salmon embryos until chronic exposure to laboratory weathered and naturally weathered oil concentrations exceeding 1,500 and 2,250 ppm, respectively, representing a total PAH tissue burden in excess of 7,100 ppb. Effluent hydrocarbons also drop well below concentrations sufficient to cause harm over the time frame of a few weeks, regardless of oiling level. Resolution of differences with Auke Bay involved the source of contributing hydrocarbons. The experimental design did not exclude dispersed oil droplets from the aqueous solution; thus, toxicity was not limited to the dissolved hydrocarbon fraction. The implications of the present results are discussed regarding the toxic risk of weathered oil to pink salmon embryos in streams of Prince William Sound (AK, USA).

Pink Salmon Spawning Habitat is Recovering a Decade after the Exxon Valdez Oil Spill

AbstractIntertidal sediment surrounding many spawning streams for pink salmon Oncorhynchus gorbuscha in western Prince William Sound, Alaska, was contaminated by the Exxon Valdez oil spill in 1989. Biochemical and egg‐dig evidence suggested that oil reduced the survival of pink salmon embryos for several years. Previous research also demonstrated that dissolved oil can be transferred to developing embryos from surrounding oiled sediment via drainage of interstitial water as a result of tidal cycling and hydraulic gradients. In this study, completed a decade after the spill, we sampled stream water for the presence of oil using passive membrane sampling devices, collected sediment and pink salmon eggs for hydrocarbon analysis, and examined alevins for induction of cytochrome P4501A (CYP1A). Polynuclear aromatic hydrocarbons (PAHs) consistent with Exxon Valdez oil were present in the water of one of six heavily impacted streams; total PAH concentrations in the stream were greatest in the lower intertidal zone. Similarly distributed total PAHs in a second stream suggested possible contamination. Oil was not detected in the remaining four streams. Induction of CYP1A in pink salmon alevins from the two contaminated streams was lowest in water above mean high tide and increased downstream. Because our samples were all selected from heavily oiled streams, we infer that most pink salmon spawning habitat either has recovered or is recovering.

K-ras oncogene DNA sequences in pink salmon in streams impacted by the Exxon Valdez oil spill: no evidence of oil-induced heritable mutations.

It was hypothesized in previous studies that the Exxon Valdez oil spill in Prince William Sound, Alaska, induced heritable mutations and resulted in mortality of pink salmon (Oncorhynchus gorbuscha) embryos. In one of these studies, laboratory exposure of pink salmon embryos to crude oil resulted in apparent mutation-induction in exon 1 and exon 2 of the K-ras oncogene, but no fish from the area impacted by the oil spill were analyzed. We assessed K-ras exon 1 and exon 2 DNA sequences in pink salmon from five streams that were oiled and five streams that were not oiled by the Exxon Valdez oil spill in Prince William Sound, and two streams with natural oil seeps and one stream without seeps on the Alaska Peninsula. Of the 79 fish analyzed for exon 1 and the 89 fish analyzed for exon 2, none had the nucleotide substitutions representing the mutations induced in the laboratory study. Other variable nucleotides occurred in similar proportions in oiled and non-oiled streams and probably represent natural allelic variation. These data do not support the hypothesis that heritable mutations in the K-ras gene were induced by the Exxon Valdez oil spill or oil seeps.

Review of Studies on Oil Damage To Prince William Sound Pink Salmon

ABSTRACT In the tenth year following the Exxon Valdez oil spill, differences of opinion still exist about injuries to pink salmon. It was alleged that exposure to oil reduced growth of fry and induced mortality in eggs. The authors reexamined the allegation that injury occurred and have concluded that insufficient consideration was given to other factors that affected results in the studies from which these allegations were drawn. The inability to track temperature differences and the unknown ages of fry precluded assessment of oil effects on growth during early marine residence. Reported higher egg mortality and long-term injury alleged to have resulted from oil exposure during incubation were confounded by the mortality of eggs that occurred as an artifact of the sampling procedure, unrelated to oil effects. The authors concluded that injury to incubating pink salmon embryos and reduced fry growth were based on an incomplete assessment of other factors that influenced these results. This evidence is supported by other research that has disclosed no oil effects on incubating eggs. Among these were studies that showed measured oil concentrations reaching the incubation substrate were 14 to 7,600 times below the lethal threshold. The seven largest runs in the history of Prince William Sound (PWS), Alaska have returned in the 10 years following the spill, which ultimately demonstrated the lack of measurable effect of the oil spill on pink salmon. The authors suggest that the allegation of oil-induced injury to PWS pink salmon needs to be reconsidered in light of these analyses.

High frequency of K‐ras mutations in pink salmon embryos experimentally exposed to Exxon valdez oil

AbstractPrevious studies demonstrated reduced survivorship of pink salmon embryos from populations in Prince William Sound, Alaska, USA, that were exposed to Exxon Valdez–released oil compared with populations from matched nonoiled streams. Survivorship was also significantly decreased in embyros from lineages that were oiled in Prince William Sound and reared in clean water under controlled hatchery conditions compared with the descendants of nonoiled lineages. This suggests that the effect of oiling on pink salmon populations was persistent and could be transmitted intergenerationally. However, the ability of environmentally released oil to cause DNA sequence alterations in natural populations has yet to be demonstrated. We used polymerase chain reaction analysis to screen for alterations in the K‐ras oncogene in DNA from pink salmon embryos that were exposed under controlled laboratory conditions to weathered Prudhoe Bay crude oil. Polymerase chain reaction and direct DNA sequence analyses were used to identify mutational hotspots within exons 1 and 2 of K‐ras, and 3′ primer mismatch analysis was used to determine the frequency of mutations in the 40 offspring of two families of pink salmon that were experimentally exposed to oiled or clean gravel. Mutations were only observed at codons 12, 13, and 61 of K‐ras, sites that are frequently mutated in animal and human tumors. All mutations resulted in deduced amino acid substitutions. As expected, in all individuals exhibiting mutations, the copy number of the normal allele exceeded that of the mutated allele. The frequencies of mutations in oiled embryos at K‐ras exons 1 and 2 were 68 and 41%, respectively. K‐ras mutations were not observed in siblings that were exposed to clean gravel or in the parents of the two experimental matings. These results indicate that exposure of pink salmon embryos to weathered Prudhoe Bay crude oil under controlled laboratory conditions can elicit somatic cell mutations in high frequency at mutational hotspots in genes such as K‐ras. However, the frequency of these events in oiled natural populations of pink salmon and other vulnerable species in Prince William Sound and the heritability of these mutations within oiled lineages have yet to be evaluated.

Sensitivity of fish embryos to weathered crude oil: Part II. Increased mortality of pink salmon (Oncorhynchus gorbuscha) embryos incubating downstream from weathered Exxon valdez crude oil

AbstractWe incubated pink salmon embryos under three exposure conditions, direct contact with oil‐coated gravel, effluent from oil‐coated gravel, and direct contact with gravel coated with very weathered oil (VWO). Embryo mortalities and polynuclear aromatic hydrocarbon (PAH) accumulation in embryo tissues during the direct‐contact and effluent exposure experiments were not significantly different, indicating that PAH accumulation was mediated by aqueous transport. Mortality rates for embryos exposed initially to a total PAH concentration (TPAH) of 1.0 ppb were significantly higher than controls when the PAH were derived from VWO. The same aqueous TPAH concentration failed to increase mortality rates when the PAH were derived from less weathered oil, indicating that toxicity of effluents from the VWO was primarily associated with the larger PAH. We conclude that water quality standards for TPAH above 1.0 ppb may fail to protect fish embryos. Further, pink salmon embryos incubating in Prince William Sound after the Exxon Valdez oil spill may have accumulated lethal concentrations of PAH from interstitial water that was contaminated when it percolated through oil reservoirs located upstream from salmon redds.

Effects of timing of stripping and female on the viability of gynogenetic and non-gynogenetic diploid pink salmon ( Oncorhynchus gorbuscha)

Timing of stripping post-ovulation and female parent have been demonstrated to affect the viability of eggs and embryos of many species of fish. Viability of gynogenetic embryos is also influenced by the female, but the effect of timing of stripping on gynogenetic survival has not been investigated. This study examined the effects of timing of stripping and female on viability of gynogenetic and non-gynogenetic diploid progeny of pink salmon. Progeny were produced using eggs successively stripped from eight female pink salmon at 1, 7, 10, and 13 days post-ovulation. Neither type of progeny's survival was significantly affected by timing of stripping. Survival of the non-gynogenetic progeny was consistently high and not significantly affected by female or the timing X female interaction. Non-gynogenetic survival rates for the interval during which most mortalities occurred, between initial pick-off at 18 h post-fertilization and eyeing, ranged from 87.4–96.8% when averaged by female. Survival rates of gynogenetic progeny for the same interval were lower and more variable, ranging from 34.0–75.2%, and were significantly affected by female and timing X female ( P < 0.05 and P < 0.01, respectively). By itself, timing of stripping does not influence the viability of pink salmon embryos. However, because of significant female and timing X female effects on survival, any attempt to improve gynogenetic production must consider the effect of the female and control timing of stripping.

Effects of transferring pink (Oncorhynchus gorbuscha) and chum (Oncorhynchus keta) salmon embryos at different developmental stages to a low incubation temperature

We transferred embryos of pink (Oncorhynchus gorbuscha) and chum (Oncorhynchus keta) salmon from 8 to 2 °C at five stages of development: 16-cell stage, blastula stage, completion of epiboly, early eye pigmentation, and late eye pigmentation. Survival rates of the embryos increased the later in development that they were transferred to 2 °C. All pink salmon blastulas transferred died, whereas 50% of chum salmon blastulas transferred survived until hatching. After epiboly was complete, survival rates of the embryos subsequently transferred to 2 °C were usually in excess of 75%. Chum salmon embryos had higher survival rates than did pink salmon embryos at all transfer stages. Significant differences were found in embryo survival rates among stocks within species and among families within stocks. Fry from early-spawning chum salmon took longer for exogenous yolk absorption ("button-up") than did those from late-spawning ones. Alevins and fry from early transfers were generally smaller than those from later ones. Different trends in embryo and alevin survival rates and alevin and fry size among stocks within species and among families within stocks were assumed to be indicative of adaptive variation to variable natural incubation environments.