We injected doses of methylmercury into the air cells of eggs of 26 species of birds and examined the dose-response curves of embryo survival. For 23 species we had adequate data to calculate the median lethal concentration (LC(50)). Based on the dose-response curves and LC(50)s, we ranked species according to their sensitivity to injected methylmercury. Although the previously published embryotoxic threshold of mercury in game farm mallards (Anas platyrhynchos) has been used as a default value to protect wild species of birds, we found that, relative to other species, mallard embryos are not very sensitive to injected methylmercury; their LC(50 )was 1.79 microg/g mercury on a wet-weight basis. Other species we categorized as also exhibiting relatively low sensitivity to injected methylmercury (their LC(50)s were 1 microg/g mercury or higher) were the hooded merganser (Lophodytes cucullatus), lesser scaup (Aythya affinis), Canada goose (Branta canadensis), double-crested cormorant (Phalacrocorax auritus), and laughing gull (Larus atricilla). Species we categorized as having medium sensitivity (their LC(50)s were greater than 0.25 microg/g mercury but less than 1 microg/g mercury) were the clapper rail (Rallus longirostris), sandhill crane (Grus canadensis), ring-necked pheasant (Phasianus colchicus), chicken (Gallus gallus), common grackle (Quiscalus quiscula), tree swallow (Tachycineta bicolor), herring gull (Larus argentatus), common tern (Sterna hirundo), royal tern (Sterna maxima), Caspian tern (Sterna caspia), great egret (Ardea alba), brown pelican (Pelecanus occidentalis), and anhinga (Anhinga anhinga). Species we categorized as exhibiting high sensitivity (their LC(50)s were less than 0.25 microg/g mercury) were the American kestrel (Falco sparverius), osprey (Pandion haliaetus), white ibis (Eudocimus albus), snowy egret (Egretta thula), and tri-colored heron (Egretta tricolor). For mallards, chickens, and ring-necked pheasants (all species for which we could compare the toxicity of our injected methylmercury with that of published reports where methylmercury was fed to breeding adults and was deposited into the egg by the mother), we found the injected mercury to be more toxic than the same amount of mercury deposited naturally by the mother. The rank order of sensitivity of these same three species to methylmercury was, however, the same whether the methylmercury was injected or maternally deposited in the egg (i.e., the ring-necked pheasant was more sensitive than the chicken, which was more sensitive than the mallard). It is important to note that the dose-response curves and LC(50)s derived from our egg injections are useful for ranking the sensitivities of various species but are not identical to the LC(50)s that would be observed if the mother bird had put the same concentrations of mercury into her eggs; the LC(50)s of maternally deposited methylmercury would be higher.
Polybrominated diphenyl ethers (PBDEs), a class of additive flame retardants, are temporally increasing in wildlife tissues and capable of disrupting normal endocrine function. We determined whether in ovo and post-hatch exposure of captive American kestrels (Falco sparverius) to environmentally relevant PBDEs alter thyroid, retinol, and oxidative stress measures. Control eggs were injected with safflower oil and subsequent nestlings fed the same vehicle; dosed eggs received PBDE congeners (BDE-47, -99, -100, -153), which mainly comprise the Penta-BDE commercial mixture, dissolved in safflower oil at concentrations (1500 ng/g total [Sigma] PBDEs) approximating those in Great Lakes gull eggs. Nestlings hatching from dosed eggs were orally exposed for 29 days to variable SigmaPBDE concentrations that are similar to levels reported in tissues of Great Lakes trout (100 ng/g). Treatment kestrels had lower plasma thyroxine (T(4)), plasma retinol, and hepatic retinol and retinyl palmitate concentrations, but unaltered triiodothyronine (T(3)) concentrations and thyroid glandular structure. BDE-47, -100, and -99 were negatively associated with plasma T(4), plasma retinol (BDE-100, -99) and hepatic retinol (BDE-47). Despite an antioxidant-rich diet, PBDE exposure induced hepatic oxidative stress, particularly in females, with an increased hepatic GSSG:GSH ratio, a marginal increase in lipid peroxidation, and increased oxidized glutathione. Positive associations were found between concentrations of BDE-183 and thiols and, in males, between BDE-99 and reduced GSH, but a negative association occurred between BDE-99 and TBARS. Subsequently, concentrations of PBDE congeners in wild birds may alter thyroid hormone and vitamin A concentrations, glutathione metabolism and oxidative stress.
Abstract-Adult mallards (Anas platyrhynchos) were fed a control diet or diets containing 10 ppm mercury as methylmercury chloride, 10 ppm selenium as seleno-DL-methionine, or 10 ppm mercury plus 10 ppm selenium. One of 12 adult males fed 10 ppm mercury died, and eight others suffered paralysis of the legs by the time the study was terminated. However, when the diet contained 10 ppm selenium in addition to the 10 ppm mercury, none of 12 males became sick. In contrast to the protective effect of selenium against mercury poisoning in males, selenium plus mercury was worse than selenium or mercury alone for some measurements of reproductive success. Both selenium and mercury lowered duckling production through reductions in hatching success and survival of ducklings, but the combination of mercury plus selenium was worse than either mercury or selenium alone. Controls produced an average of 7.6 young per female, females fed 10 ppm selenium produced an average of 2.8 young, females fed 10 ppm mercury produced 1.1 young, and females fed both mercury and selenium produced 0.2 young. Teratogenic effects also were worse for the combined mercury plus selenium treatment; deformities were recorded in 6.1% of the embryos of controls, 16.4% for those fed methylmercury chloride, 36.2% for those fed selenomethionine, and 73.4% for those fed methylmercury chloride and selenomethionine. The presence of methylmercury in the diet greatly enhanced the storage of selenium in tissues. The livers of males fed 10 ppm selenium contained a mean of 9.6 ppm selenium, whereas the livers of males fed 10 ppm selenium plus 10 ppm mercury contained a mean of 114 ppm selenium. However, selenium did not enhance the storage of mercury. The results show that mercury and selenium may be antagonistic to each other for adults and synergistic to young, even within the same experiment.
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