Morphometric abnormalities in brains of great blue heron hatchlings exposed in the wild to PCDDs.

Abstract-Effects of PCBs were studied in common terns (Sterna hirundo).Hatchlings from eggs collected from Dutch breeding colonies and incubated artificially were raised to an age of 21 d. The birds were fed fish spiked with PCB 126 alone or in combination with PCB 153 (1:1,000), resulting in concentrations in the food ranging from 0.01 to 1.2 ng toxic equivalents (TEQs)/g wet weight.The most sensitive effect parameter was induction of hepatic CYP1A-associated ethoxyresorufin-O-deethylation (EROD) activity, and a nonlinear concentration-effect relationship could be determined with the TEQ concentration (r ϭ 0.967, p Ͻ 0.001). Induction of pentoxyresorufin-O-depenthylation and methoxyresorufin-O-demethylation activities was observed at dose levels similar to those that induced EROD activity. The estimated lowest-observed-effect level for induction of CYP1A in the common tern was approx. 25 ng TEQ/g liver lipid, which was caused by concentrations in the food of approx. 0.6 ng TEQ/g fish wet weight. At these concentrations, a 50% reduction in plasma total thyroxine compared with controls also was observed. Concentrations of plasma total thyroxine were negatively correlated with hepatic TEQ concentrations (r ϭ 0.523, p Ͻ 0.01), but the shape of the nonlinear concentration-effect relationship did not allow determination of a lowest-observed-effect level. No changes were found for hepatic hydroxylation of testosterone. Bursa weight decreased proportionally to hepatic concentrations of TEQs (r ϭ 0.433, p Ͻ 0.05) and showed a similar sensitivity as that observed for EROD activity. Concentrations of TEQs in The Netherlands are approx. 0.1 ng TEQ/g wet weight fish, which is approximately six times lower than the lowest-observed-effect level for CYP1A induction in terns as estimated in this study. It is concluded that no overt effects on growth and development in the common tern are expected with this background exposure during the posthatch period.

Section: Discussionmentioning

confidence: 99%

Biochemical and developmental effects of dietary exposure to polychlorinated biphenyls 126 and 153 in common tern chicks (Sterna hirundo)

Bosveld

Nieboer

Bont

et al. 2000

“…Herons. The first studies [16,17] examined the brains of great blue heron hatchlings taken as eggs from relatively contaminated and relatively uncontaminated colonies in the Strait of Georgia, British Columbia, Canada. For these studies, two pair‐matched sibling eggs were taken from each nest.…”

Section: Methodsmentioning

confidence: 99%

Developmental neurotoxic effects of dioxin and dioxin‐like compounds on domestic and wild avian species

Henshel

1998

Abstract-In ovo exposure to dioxin and dioxin-like compounds has been shown to be associated with the development of grossly asymmetric avian brains. This asymmetry is primarily seen in two major brain regions, the forebrain and the tectum, and is detectable in the intact (but isolated) brain or in cross sections, as in computer tomographic (CT) images of the brain. Brain asymmetry has been observed in several wildlife species (heron, cormorant, and eagle) exposed to a mixture of contaminants in the wild, as well as in a domestic species (chicken) exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in ovo under controlled conditions. Asymmetry appears with increasing frequency and severity in embryos and hatchlings exposed to increasing doses of TCDD beginning early in embryonic development. Since asymmetry is evident in early embryos (embryonic day 9) when the braincase is just a thin covering, it is unlikely that brain asymmetry is caused by effects on the braincase rather than on the brain itself. In addition, preliminary histological evaluation of heron hatchling brains indicates that the pyriform (striate) cortex has increased cell density in contaminated versus control brains, although it is not yet clear whether this change in cell density is also manifested asymmetrically. Immunohistochemical analysis of embryonic chicken spinal cord demonstrated that TCDD exposure in ovo also induces a dysmyelination.

“…Measurements of brain morphology were made as per Henshel et al [10,31]. In summary, the width, angle, height, and depth of the right and left side of each brain were measured using an engineering ruler with 0.5‐mm gradations.…”

Section: Methodsmentioning

confidence: 99%

Contaminant concentrations and biomarker response in great blue heron eggs from 10 colonies on the upper Mississippi River, USA

Custer¹,

Hines²,

Melancon³

et al. 1997

Abstract-In 1993, great blue heron (Ardea herodias; GBH) eggs were collected from 10 colonies on the upper Mississippi River (UMR). They were then artificially incubated until pipping and analyzed for mercury, selenium, and organochlorines. Livers of embryos were analyzed for hepatic microsomal ethoxyresorufin-O-dealkylase (EROD) activity and four measures of oxidative stress. Brains were measured for asymmetry and blood was measured for the coefficient of variation of DNA (DNA CV). Organochlorine concentrations were generally low (geometric mean DDE ϭ 1.3 g/g wet weight; polychlorinated biphenyl [PCB] ϭ 3.0 g/g; 2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD] ϭ 11.5 pg/g). Eggshell thickness was negatively correlated with DDE concentrations. Mercury (geometric mean ϭ 0.8 g/g dry weight) and selenium (3.1 g/g dry weight) concentrations in GBH eggs were within background levels. EROD activity was not correlated with total PCBs, TCDD, or toxic equivalents (TEQs), based on the relative contribution of individual PCB congeners, dibenzodioxins (PCDDs), and dibenzofurans (PCDFs) to total calculated TEQs. Three of the four measures of oxidative stress were correlated with mercury concentrations. Twenty of 43 (47%) embryo brains were asymmetrical and the embryos with asymmetrical brains had higher EROD concentrations in the liver and higher DNA CV in the blood than embryos with symmetrical brains.