Abstract
We observed a slight drop in the growth of Xenopus laevis and Pseudacris triseriata larvae following acute exposure (24-48 h) during egg development to three concentrations of TCDD (0.3, 3.0, 30.0 microg/l). Our exposure protocol was modeled on a previous investigation that was designed to mimic the effects of maternal deposition of TCDD. The doses selected were consistent with known rates of maternal transfer between mother and egg using actual adult body burdens from contaminated habitats. Egg and embryonic mortality immediately following exposure increased only among 48 h X. laevis treatments. Control P. triseriata and X. laevis completed metamorphosis more quickly than TCDDtreated animals. The snout-vent length of recently transformed P. triseriata did not differ between treatments although controls were heavier than high-dosed animals. Likewise, the snout-vent length and weight of transformed X. laevis did not differ between control and TCDD treatments. These findings provide additional evidence that amphibians, including P. triseriata and X. laevis are relatively insensitive to acute exposure to TCDD during egg and embryonic development. Although the concentrations selected for this study were relatively high, they were not inconsistent with our current understanding of bioaccumulation via maternal transfer.
Highlights
In recent years many amphibian populations worldwide have experienced a dramatic and well-documented decline
Gutleb et al [56] documented a dose-dependent increase in tail and eye deformities among X. laevis but not R. temporaria larvae following long-term oral exposure to polychlorinated biphenyls (PCBs). These findings suggest that ranid tadpoles may be less susceptible to polyhalogenated aromatic hydrocarbons (PHAHs)-mediated malformations than X. laevis [56] and are consistent with earlier trials in which other ranid species appear relatively insensitive to TCDD exposure [68]
The results our study provide additional evidence that amphibians are relatively insensitive to acute exposure to TCDD even at relatively high concentrations [40, 45]
Summary
In recent years many amphibian populations worldwide have experienced a dramatic and well-documented decline. TCDD-induced toxicity is largely mediated through the cytoplasmic aryl hydrocarbon receptor (AhR) which is present in all vertebrates [17]. Upon binding in the cytoplasm, the AhR protein translocates to the nucleus, sheds its chaperone proteins and forms a heterodimer with ARNT (AhR nuclear translocator) [19,20,21,22,23]. This complex regulates the transcription of target genes including cytochrome CYP1A1 (P4501A1), CYP1B1, and NADPH quinone oxidoreductase by binding to cis-acting DNA elements (xenobiotic response elements; XREs) [23,24,25]. Maternal exposure to TCDD in rats results in offspring with reduced body weight [30,31,32], genital dysmorphogenesis and decreased fertility [32]
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