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Histopathological changes in the hepatopancreas of the penaeid shrimp Metapenaeus dobsoni exposed to petroleum hydrocarbons

机译:暴露于石油烃的对虾虾新对虾的肝胰腺的组织病理学变化

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摘要

Petroleum hydrocarbons are toxic to marine invertebrates when present above a threshold level in the marineudecosystem. The major detoxification organ in shrimps is the hepatopancreas, which has been used as an indicator organ for toxicity assessment. The effects of Bombay High Crude on the morphology of hepatopancreatic tubules of Metapenaeus dobsoni when examined under the light and electron microscopes reveal a series of changes indicating that the cellular compensatory mechanism is activated by low or sub lethal doses of hydrocarbons. At the high sub lethal dose of 8 ppm the cellular detoxification mechanisms fail resulting in severe structural damage. The changes indicate that they are dose and time related histopathological responses. Changes such as an increased presence of B - cells towards the distal end of the tubule,udsubstantial increase in the number of F/B cells, extensive cytrorrhexis, reduction in the number of E- cells.udvacuolation of E-, R- and F- cells are changes which can be detected under light microscope along with theudpresence of pyknotic nuclei, storage of large lipid droplet in combination with cells voided of other subcellularudcomponents, proliferation and distortion of Golgi apparatus and mitochondria which were detected in the ultrastructure study can be used as biomarkers of stress caused by petroleum hydrocarbon pollution.
机译:当在海洋生物系统中的阈值水平以上存在时,石油烃对海洋无脊椎动物有毒。虾的主要排毒器官是肝胰腺,它已被用作毒性评估的指示器官。在光学和电子显微镜下观察时,孟买高原油对多巴对虾肝胰腺小管形态的影响揭示了一系列变化,表明细胞代偿机制是由低剂量或低致死剂量的碳氢化合物激活的。在8 ppm的高亚致死剂量下,细胞排毒机制失效,导致严重的结构破坏。这些变化表明它们是剂量和时间相关的组织病理学反应。变化,例如朝向肾小管远端的B细胞增多, F / B细胞数量大量增加,广泛的膀胱溢液,E细胞数量减少。 E-,R- F细胞和F细胞是可以在光学显微镜下检测到的变化,包括状核的不存在,大脂质滴的储存以及与其他亚细胞的无细胞成分结合的细胞的结合,高尔基体和线粒体的增殖和变形。超微结构研究可以用作石油烃污染引起的压力的生物标志。

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