Acid precipitation can have a harmful effect on aquatic birds, due in part to increases in aluminum availability. Young rapidly growing (broiler strain) chickens were used as a model to examine the effects of aluminum and acid on growth and circulating concentrations of adrenocorticol hormones. Two concentrations of acid (sulfuric acid) or aluminum (aluminum sulfate) or sodium sulfate were administered to a heavy (broiler) strain of chickens for 10 days (Days 4 to 14 of age). Additional treatment groups included a control diet either fed ad libitum or pair-fed relative to the chicks on the acid or aluminum diets. Compared with the chicks receiving the control diet ad libitum, growth (body weight) was reduced in chicks on the aluminum (high and low level), acid (high level), and sodium sulfate (high level) treatments and the respective pair-fed groups. Circulating concentrations of corticosterone (B) were elevated in the chicks receiving the high dose of aluminum and the respective pair-fed control when compared with the chicks which had free access to the control diet. Thus, the increase in plasma B appears to be linked to the low food intake and not to the A1 per se. Circulating concentrations of aldosterone were increased in the chicks receiving either the high dose of aluminum or the acid relative to chicks fed the control diet (both ad libitum or pair-fed controls). However, circulating concentrations of aldosterone were unaffected by either dose of sodium sulfate employed. Thus, the increase in plasma aldosterone appears to be specific to the metabolic acidosis created by A1 or acid. It is concluded that environmental acid may either directly or indirectly influence adrenocortical function. Moreover, the present study provides evidence for the independent control of circulating concentrations of corticosterone and aldosterone in the chicken.
"The intraassay coefficient of variance (CV) and interassay CV were 10.1% and 10.9%, respectively. Plasma concentrations of corticosterone and aldosterone were determined to assess stress levels and identify atrazine-influenced changes in sodium balance using the method of Capdevielle et al. (1996). Blood samples for corticosterone analysis were taken 30 min following the last daily subcutaneous injection of atrazine to assess changes in adrenal cortical hormone secretion (study 4) and in quail implanted for 14 days with atrazine to examine chronic changes. "
[Show abstract][Hide abstract] ABSTRACT: The widely used herbicide, atrazine, has been reported to exhibit reproductive toxicity in rats and amphibians. The present studies investigate toxicity of atrazine in Japanese quail and its ability to influence reproduction in sexually immature females. Atrazine was administered in the diet at concentrations from 0.001 to 1000 ppm (approximately 109 mg kg-1 per day) or systemically via daily subcutaneous injections (1 and 10 mg kg-1) or Silastic implants. Atrazine did not cause overt toxicity in sexually immature female quail (no effects on change in body weight, feed intake, mortality or on circulating concentrations of the stress hormone, corticosterone). It was hypothesized that if atrazine were to have estrogenic activity or to enhance endogenous estrogen production, there would be marked increases in the weights of estrogen sensitive tissues including the oviduct, the liver and the ovary together with changes in gonadotropin secretion. However, atrazine had no effect on either liver or ovary weights. Atrazine in the diet increased oviduct weights at 0.1 and 1 ppm in some studies. These effects were not consistently observed and were not significant when data from studies were combined. Systemic administration of atrazine had no effect on oviduct weights. Dietary (concentrations from 0.001 to 1000 ppm) and systemically administered atrazine had no effect on circulating concentrations of luteinizing hormone (LH). The present studies provide evidence for a lack of general or reproductive toxicity of atrazine in birds.
[Show abstract][Hide abstract] ABSTRACT: There have been significant strides in our knowledge of the effects of toxicants on birds. This communication presents a brief review of avian toxicology with emphasis on effects of common toxicants that disrupt endocrine system function and control of reproduction, growth, development, stress and calcium-phosphorus homeostasis. For those hormonal systems that act through hypothalamic-pituitary axes, we emphasize current knowledge of the axis ``level'' at which the toxicants alter endocrine control. The classes of toxicants discussed are acid rain and/or aluminum, organochlorines such as polychlorinated biphenyls (PCBs), fungicides and insecticides, mycotoxins, (PCBs) and petroleum. The use of several types of avian models for endocrine disruption studies is discussed in the context of utility and practicality, developmental modes, species sensitivity and the choice of sentinel species. Promising new approaches for avian toxicological research are considered including shell-less embryos, continuous-flow administration of toxicants to avian embryos, gene microarrays, proteomics and metabolomics.
Elizabeth A Tibbetts, Taylor Forrest, Cassondra Vernier, Judy Jinn, Andrew Madagame
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