In ovo inhibition of steroid metabolism by bisphenol-A as a potential mechanism of endocrine disruption.

During embryonic development, endogenous signals, for example steroid hormones, and exogenous signals, for example endocrine disrupting chemicals (EDCs), have the capacity to produce phenotypic effects that persist into adulthood. As the actions of steroids are mediated through the binding of steroid receptors, most studies of EDCs have assumed that they too elicit their effects by binding steroid receptors. We tested an alternative hypothesis, namely that EDCs elicit their effects during embryonic development by disrupting the metabolism of maternally derived steroids, thereby allowing maternally derived steroids to bind steroid receptors and elicit effects. Specifically, we examined the ability of the EDC, bisphenol-A (BPA) to inhibit the normal metabolism of oestradiol during the first nine days of embryonic development in the red-eared slider turtle (Trachemys scripta). We found that, when BPA was present, oestrogen metabolism was inhibited when compared to control eggs. In particular, the formation of oestrone sulfate was blocked in BPA-treated eggs. We postulate that the oestrogenic effects of EDCs may be driven, at least in part, by inappropriate oestrogen signalling. The retention of oestrogens at points of development when they would normally be metabolized to inactive forms might also help explain low-dose effects frequently reported for EDCs.

Humoral immune responses are maintained with age in a long-lived ectotherm, the red-eared slider turtle.

Aging is typically associated with a decrease in immune function. However, aging does not affect each branch of the immune system equally. Because of these varying effects of age on immune responses, aging could affect taxa differently based on how the particular taxon employs its resources towards different components of immune defense. An example of this is found in the humoral immune system. Specific responses tend to decrease with age while non-specific, natural antibody responses increase with age. Compared with mammals, reptiles of all ages have a slower and less robust humoral immune system. Therefore, they may invest more in non-specific responses and thus avoid the negative consequences of age on the immune system. We examined how the humoral immune system of reptiles is affected by aging and investigated the roles of non-specific, natural antibody responses and specific responses by examining several characteristics of antibodies against lipopolysaccharide (LPS) in the red-eared slider turtle. We found very little evidence of immunosenescence in the humoral immune system of the red-eared slider turtle, Trachemys scripta, which supports the idea that non-specific, natural antibody responses are an important line of defense in reptiles. Overall, this demonstrates that a taxon's immune strategy can influence how the immune system is affected by age.

No evidence that estrogens affect the development of the immune system in the red-eared slider turtle, Trachemys scripta.

Exposure to maternally derived substances during development can affect offspring phenotype. In ovo exposure to maternally derived steroids has been shown to influence traits such as growth and behavior in the offspring. The development of the immune system also can be altered by exposure to both androgens and glucocorticoids in a variety of species, but much less is known about the potential for estrogens to influence the development of this system. We examined the effect of estradiol on the development of both innate and adaptive immune components in the red-eared slider turtle (Trachemys scripta). A bacterial killing assay was used to assess innate immunity, a delayed-type hypersensitivity test for cellular immunity, and total immunoglobulin levels to measure the humoral immune response. We found no effect of in ovo estradiol treatment on any of our immune measures despite using doses that are known to influence other phenotypic parameters during development and varying the timing of dosing across development. Our results suggest that maternally derived estradiol does not affect the development of the immune system in T. scripta.

Experimentally increased in ovo testosterone leads to increased plasma bactericidal activity and decreased cutaneous immune response in nestling house wrens.

Maternally derived testosterone in the eggs of birds may benefit nestlings by increasing various aspects of their growth, condition and behavioral development, but these benefits may come at a cost, including suppression of immune responsiveness. Experiments on a variety of species in which in ovo levels of testosterone have been experimentally increased have produced mixed results; some have found increased growth and suppressed immune function of nestlings whereas others have found the opposite. In an attempt to clarify the relationship between in ovo testosterone and nestling size, mass, health state and immune responsiveness, we experimentally increased levels of testosterone in the eggs of house wrens (Troglodytes aedon). We simultaneously determined the size, mass, hematocrit (a measure of health state), cutaneous immune response to phytohaemagglutinin and plasma bactericidal activity of nestlings near the time of fledging. We predicted that nestlings hatching from testosterone-injected eggs would exhibit lower immune responsiveness, but achieve greater mass, size and condition, than nestlings hatching from vehicle-injected control eggs. Instead, we found that nestlings hatching from testosterone-injected eggs had a weaker cutaneous immune response but greater bactericidal activity than those hatching from control eggs. They did not, however, differ significantly in mass, size or hematocrit from controls. These results suggest that experimentally increased in ovo testosterone induced a trade-off between bactericidal activity and the cutaneous immune response. The opposite responses by two different measures of immune function to experimentally increased in ovo testosterone underscore the importance of including multiple immune assays when investigating the potential for trade-offs with the immune system and other physiological functions.