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Evaluating the Stress Response as a Bioindicator of Sub-Lethal Effects of Crude Oil Exposure in Wild House Sparrows (Passer domesticus)

机译:评价应激反应作为野生麻雀(Passer domesticus)原油暴露的次致命影响的生物指示剂

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摘要

Petroleum can disrupt endocrine function in humans and wildlife, and interacts in particularly complex ways with the hypothalamus-pituitary-adrenal (HPA) axis, responsible for the release of the stress hormones corticosterone and cortisol (hereafter CORT). Ingested petroleum can act in an additive fashion with other stressors to cause increased mortality, but it is not clear exactly why—does petroleum disrupt feedback mechanisms, stress hormone production, or both? This laboratory study aimed to quantify the effects of ingested Gulf of Mexico crude oil on the physiological stress response of house sparrows (Passer domesticus). We examined baseline and stress-induced CORT, negative feedback, and adrenal sensitivity in house sparrows given a 1% oil or control diet (n = 12 in each group). We found that four weeks on a 1% oil diet did not alter baseline CORT titers or efficacy of negative feedback, but significantly reduced sparrows' ability to secrete CORT in response to a standardized stressor and adrenocorticotropin hormone injection, suggesting that oil damages the steroid-synthesizing cells of the adrenal. In another group of animals on the same 1% oil (n = 9) or control diets (n = 8), we examined concentrations of eight different blood chemistry parameters, and CORT in feathers grown before and during the feeding experiments as other potential biomarkers of oil exposure. None of the blood chemistry parameters differed between birds on the oil and control diets after two or four weeks of feeding, nor did feather CORT differ between the two groups. Overall, this study suggests that the response of CORT to stressors, but not baseline HPA function, may be a particularly sensitive bioindicator of sub-lethal chronic effects of crude oil exposure.
机译:石油会破坏人类和野生动植物的内分泌功能,并以特别复杂的方式与下丘脑-垂体-肾上腺(HPA)轴相互作用,从而导致压力激素皮质酮和皮质醇(以下称为CORT)的释放。摄入的石油可以与其他应激源相加,从而导致死亡率增加,但尚不清楚确切的原因-石油会破坏反馈机制,应激激素产生还是两者同时发生?这项实验室研究旨在量化摄取的墨西哥湾原油对麻雀(Passer domesticus)的生理应激反应的影响。我们检查了基线和压力诱导的CORT,负反馈以及在食用1%油或对照饮食的情况下麻雀的肾上腺敏感性(每组n = 12)。我们发现,以1%的油脂饮食食用4周不会改变基线CORT滴度或负面反馈的功效,但会显着降低麻雀对标准化应激源和促肾上腺皮质激素激素注射的反应而分泌CORT的能力,这表明油脂会损害类固醇-合成肾上腺细胞。在另一组使用相同的1%油(n = 9)或对照饮食(n = 8)的动物中,我们检查了八种不同血液化学参数的浓度,以及在喂养实验之前和期间生长的羽毛中的CORT作为其他潜在的生物标记物油暴露。喂食两到四个星期后,食用油的鸡和对照饮食之间的血液化学参数没有差异,两组的羽毛CORT也没有差异。总体而言,这项研究表明,CORT对应激源的反应而非基线HPA功能的反应,可能是对原油暴露造成的亚致死慢性影响的特别敏感的生物指标。

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