Coastal
reintroduction sites for California condors (Gymnogyps
californianus) can lead to elevated halogenated
organic compound (HOC) exposure and potential health impacts due to
the consumption of scavenged marine mammals. Using nontargeted analysis
based on comprehensive two-dimensional gas chromatography coupled
to time-of-flight mass spectrometry (GC×GC/TOF-MS), we compared
HOC profiles of plasma from inland and coastal scavenging California
condors from the state of California (CA), and marine mammal blubber
from CA and the Gulf of California off Baja California (BC), Mexico.
We detected more HOCs in coastal condors (32 ± 5, mean number
of HOCs ± SD, n = 7) than in inland condors
(8 ± 1, n = 10) and in CA marine mammals (136
± 87, n = 25) than in BC marine mammals (55
± 46, n = 8). ∑DDT-related compounds,
∑PCBs, and total tris(chlorophenyl)methane (∑TCPM) were,
respectively, ∼7, ∼3.5, and ∼148 times more abundant
in CA than in BC marine mammals. The endocrine-disrupting potential
of selected polychlorinated biphenyls (PCB) congeners, TCPM, and TCPMOH
was determined by in vitro California condor estrogen receptor (ER)
activation. The higher levels of HOCs in coastal condors compared
to those in inland condors and lower levels of HOC contamination in
Baja California marine mammals compared to those from the state of
California are factors to consider in condor reintroduction efforts.
Recently, California condors (Gymnogyps californianus) have been reintroduced to coastal regions of California where they feed on marine mammal carcasses. There is evidence that coastal-dwelling condors experience reproductive issues, such as eggshell thinning, likely resulting from exposure to endocrine-disrupting chemicals (EDCs). To address this problem, we have identified and cloned condor estrogen receptors (ESRs) 1 and 2 and characterized their activation by EDCs present in the coastal habitats where condors reside. Dichlorodiphenyltrichloroethane (DDT) and its metabolites all activated ESR1 and ESR2, although their relative potency differed between the receptors. Bisphenol A, dieldrin, trans-nonachlor, and polychlorinated biphenyl 52 (PCB52) moderately activated both ESRs, whereas PCB138 and PCB153 stimulated little to no activation. Overall, EDC activation of condor ESR2, which is the first ESR2 cloned from a raptor species, was greater than that of ESR1. Significant activation of both condor ESRs by EDCs occurred at high concentrations (≥1μM), which are within the range of plasma levels of certain EDCs (eg, dichlorodiphenyldichloroethylene [p'p-DDE]) in coastal-dwelling condors. Finally, phylogenetic analyses of ESRs of 41 avian species identified a single amino acid position in ESR2 under positive selection. Mutation of this amino acid affected receptor activation by EDCs, suggesting the identity of this amino acid may influence EDC sensitivity of avian species. Together, these findings broaden our understanding of EDC interactions with ESRs in avian species. For condors specifically, these data could be used to evaluate EDC exposure risk at future release sites to identify those least likely to compromise the continued recovery of this species.
Lack of ovulation is common in captive southern white rhino females and contributes to poor reproductive success. We show that ovulation can be induced efficiently with exogenous hormones using a single treatment protocol. This information can lead to improved genetic management of captive populations acting as insurance against extinction.
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