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ABSTRACT: Domestic chickens (Gallus gallus) are an excellent model in which to evaluate developmental toxicity and oxidative stress because of their high sensitivity to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The goal of this study was to measure the effects of environmentally relevant doses of TCDD on endogenous hepatic antioxidant enzyme activity in hatchling chickens. The vehicle (sunflower oil) or 2, 20, or 200 pg/g TCDD was injected into chicken eggs before incubation. On hatching, livers were harvested and quickly frozen. The changes in activity of antioxidant enzymes, including glutathione peroxidase (GPx), glutathione reductase (GRx), copper zinc superoxide dismutase (SOD), and catalase (CAT) were determined as indicators of oxidative stress. TCDD exposure was associated with a significant suppression of the activities of the protective endogenous enzymes GPx, GRx, and SOD in the liver, even at the lowest dose. CAT activity was also suppressed, but not significantly. The measured decreases were 37% to 63% for GPx, 50% to 58% for GRx, 30% to 40% for SOD, and 16% to 24% for CAT. Noncomplex dose-response relationships were evident in GPx and GRx, whereas SOD and CAT curves were U-shaped. These results demonstrate that a decreased ability to scavenge reactive oxygen species may result from developmental TCDD exposure at very low doses, contributing to oxidative stress and thus to the embryotoxicity of TCDD.
Archives of Environmental Contamination and Toxicology 06/2007; 52(4):590-5. · 1.93 Impact Factor
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ABSTRACT: Previous studies have indicated that in ovo exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds is correlated with the development of grossly asymmetric brains. This asymmetry is manifested as a difference between the two halves of the forebrain and the tecta. Previously, only wildlife species (heron, cormorant, and eagle) had been shown to manifest this response. In the wildlife studies, the frequency and degree of left-right interhemispheric differences had been correlated with the levels of polychlorinated dibenzo-p-dioxin toxic equivalency factors (TEFs) in eggs from the same nest (heron, cormorant). We studied the effect of in ovo exposure to TCDD on the brain throughout development in a sensitive laboratory model (chicken). Embryos from chicken eggs (Gallus gallus) injected with one of several doses of TCDD or vehicle control were sacrificed after 9, 11, 13, 15, 17, or 20 days of incubation, or incubated to hatch and then sacrificed either within 24 hr or at 3 weeks post-hatch. Measurements of both chicken embryo and hatchling brains indicated that 1) TCDD alone induced the brain asymmetry in developing chickens; 2) this brain asymmetry was similar to that observed in animals exposed in the wild to a mixture of TCDD-related contaminants; 3) there was a dose-related increase in both the frequency and severity of brain asymmetry observed at all ages measured; and 4) the asymmetry was measurable in embryonic brains at an age when the braincase was a thin, flexible layer (embryonic day 9), implying that the effect of TCDD was directly on the developing brain and not indirectly via an effect on the braincase.
Environmental Health Perspectives 08/1997; 105(7):718-25. · 7.04 Impact Factor
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Diseases of the nervous system 08/1961; 22:396-8.
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Veterinary medicine 05/1946; 41:178.
