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Chronic exposure to a low dose of ingested petroleum disrupts corticosterone receptor signalling in a tissue-specific manner in the house sparrow (Passer domesticus)

机译:长期暴露于低剂量摄入的石油中麻雀(Passer domesticus)以组织特异性的方式破坏了皮质酮受体的信号传导

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摘要

Stress-induced concentrations of glucocorticoid hormones (including corticosterone, CORT) can be suppressed by chronic exposure to a low dose of ingested petroleum. However, endocrine-disrupting chemicals could interfere with CORT signalling beyond the disruption of hormone titres, including effects on receptors in different target tissues. In this study, we examined the effects of 6 weeks of exposure to a petroleum-laced diet (1% oil weight:food weight) on tissue mass and intracellular CORT receptors in liver, fat, muscle and kidney (metabolic tissues), spleen (an immune tissue) and testes (a reproductive tissue). In the laboratory, male house sparrows were fed either a 1% weathered crude oil (n = 12) or a control diet (n = 12); glucocorticoid receptors and mineralocorticoid receptors were quantified using radioligand binding assays. In oil-exposed birds, glucocorticoid receptors were lower in one metabolic tissue (liver), higher in another metabolic tissue (fat) and unchanged in four other tissues (kidney, muscle, spleen and testes) compared with control birds. We saw no differences in mineralocorticoid receptors between groups. We also saw a trend towards reduced mass of the testes in oil-exposed birds compared with controls, but no differences in fat, kidney, liver, muscle or spleen mass between the two groups. This is the first study to examine the effects of petroleum on CORT receptor density in more than one or two target tissues. Given that a chronic low dose of ingested petroleum can affect stress-induced CORT titres as well as receptor density, this demonstrates that oil can act at multiple levels to disrupt an animal’s response to environmental stressors. This also highlights the potential usefulness of the stress response as a bioindicator of chronic crude oil exposure.
机译:长期暴露于低剂量摄入的石油中,可以抑制应激诱导的糖皮质激素的浓度(包括皮质酮,CORT)。但是,破坏内分泌的化学物质可能会干扰CORT信号传导,而不仅仅是破坏激素滴度,包括对不同靶组织受体的影响。在这项研究中,我们检查了暴露于石油盐饮食(1%油重:食物重量)6周后对肝脏,脂肪,肌肉和肾脏(新陈代谢组织),脾脏(免疫组织)和睾丸(生殖组织)。在实验室中,给雄麻雀喂食1%风化的原油(n = 12)或对照饮食(n = 12)。糖皮质激素受体和盐皮质激素受体使用放射性配体结合测定法定量。与对照鸟类相比,在暴露于油的鸟类中,一个代谢组织(肝脏)中的糖皮质激素受体较低,在另一个代谢组织(脂肪)中的糖皮质激素受体较高,而在其他四个组织(肾脏,肌肉,脾脏和睾丸)中的糖皮质激素受体却没有变化。我们发现两组之间的盐皮质激素受体没有差异。我们还发现,与对照组相比,接触过油的鸟类的睾丸质量有减少的趋势,但两组之间的脂肪,肾脏,肝脏,肌肉或脾脏质量没有差异。这是第一个研究石油对一个或两个以上目标组织中CORT受体密度的影响的研究。鉴于长期摄入的低剂量石油会影响压力诱发的CORT滴度以及受体密度,因此表明油可以在多个水平上起作用,破坏动物对环境应激源的反应。这也凸显了应激反应作为长期暴露于原油的生物指标的潜在用途。

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