Summary: | Several recent studies suggest that the prevalence of limb abnormalities in North American anurans is elevated compared to historical records. These obsrvations have caused concern that environmental conditions are responsible for the increase through perturbation of normal limb development. Two of the hypothesized causes of the observed developmental abnormalities are chemical intoxication and ultraviolet radiation. Initially, chemicals which could mimic the action of retinoic acid RA), were of concern. Normal limb development is dependent on the proper spatial and temporal concentrations of RA in the limb field and numerous mammalian, amphibian, and avian studies have demonstrated that excess RA administered at specific developmental intervals can result in limb dysmorphogenesis. Generally, these effects are characterized as deletions, but some evidence suggests that RA administration can cause supernumerary limbs as well. The types of limb effects observed in the RA studies are generally consistent with the malformations observed in amhibian limbs in the field. Based on this similarity, it was hypothesized that an unknown-chemical which acts as a RA receptor agonist may be the cause of limb malformations observed in native anuran populations. may be the cause of limb malformations observed in native anuran populations. To test this hypotheses, several anuran species were exposed to ambient levels of solar UB-B from the pre-blastuls stage through metamprohosis. Exposure to solar UV-B results exclusively in terminal truncations of the limbs. The effecs are observed at every level in the limb, but are more prevalent in the distal limb segments. Although deletions are the most commonly observed malformation in the field, qualitative differences exist between the deletions observed in the field to those generated by controlled UV-B exposure, creating uncertainty about the contribution of UV-B to amphibian limb malformations. hypothesis, we exposed several species of anurans to archetypical ligand of the RA receptor, all-trans-retinoic acid, using pulse exposures during sensitive developmental intervals and by conducting chronic exposures from the blastula stage through metamorphosis. The results demonstrate that pulse exposures cause limb dysmorphogensis in all species tested, but that chronic exposures do not result in limb dysmorphogenesis at concentrations that permit survival. These studies suggest that aqueous exposures to agonists of the RA pathway are unlikely to cause limb malformations in wild populations of native anurans. An alternate non-chemical hypothesis is that exposure to ultraviolet-B-ratiation (UV-B), which has increased due to stratospheric ozone depletion, causes limb
|