首页> 美国卫生研究院文献>Wiley-Blackwell Online Open >A primary phosphorus‐deficient skeletal phenotype in juvenile Atlantic salmon Salmo salar: the uncoupling of bone formation and mineralization
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A primary phosphorus‐deficient skeletal phenotype in juvenile Atlantic salmon Salmo salar: the uncoupling of bone formation and mineralization

机译:大西洋鲑鲑Salmo salar中主要的缺磷骨骼型:骨形成和矿化的解耦

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摘要

To understand the effect of low dietary phosphorus (P) intake on the vertebral column of Atlantic salmon Salmo salar, a primary P deficiency was induced in post‐smolts. The dietary P provision was reduced by 50% for a period of 10 weeks under controlled conditions. The animal's skeleton was subsequently analysed by radiology, histological examination, histochemical detection of minerals in bones and scales and chemical mineral analysis. This is the first account of how a primary P deficiency affects the skeleton in S. salar at the cellular and at the micro‐anatomical level. Animals that received the P‐deficient diet displayed known signs of P deficiency including reduced growth and soft, pliable opercula. Bone and scale mineral content decreased by c. 50%. On radiographs, vertebral bodies appear small, undersized and with enlarged intervertebral spaces. Contrary to the X‐ray‐based diagnosis, the histological examination revealed that vertebral bodies had a regular size and regular internal bone structures; intervertebral spaces were not enlarged. Bone matrix formation was continuous and uninterrupted, albeit without traces of mineralization. Likewise, scale growth continues with regular annuli formation, but new scale matrix remains without minerals. The 10 week long experiment generated a homogeneous osteomalacia of vertebral bodies without apparent induction of skeletal malformations. The experiment shows that bone formation and bone mineralization are, to a large degree, independent processes in the fish examined. Therefore, a deficit in mineralization must not be the only cause of the alterations of the vertebral bone structure observed in farmed S. salar. It is discussed how the observed uncoupling of bone formation and mineralization helps to better diagnose, understand and prevent P deficiency‐related malformations in farmed S. salar.
机译:为了了解饮食中低磷摄入量对大西洋鲑鲑鲑鱼脊椎骨柱的影响,在后软体动物中诱发了原发性磷缺乏症。在受控条件下,在10周的时间内饮食中的P含量降低了50%。随后通过放射学,组织学检查,骨骼和鳞片中矿物质的组织化学检测以及化学矿物质分析对动物的骨骼进行分析。这是第一个关于原发性磷缺乏症如何在细胞和微观解剖学水平影响唾液链球菌骨骼的研究。饮食中缺乏P的动物表现出已知的P缺乏迹象,包括生长减慢和柔韧的盖。骨和鳞片矿物质含量降低了c。 50%。在X光片上,椎体看起来很小,尺寸过小,并且椎间间隙增大。与基于X射线的诊断相反,组织学检查显示椎体具有规则的大小和规则的内部骨骼结构。椎间隙未扩大。骨基质的形成是连续且不间断的,尽管没有矿化的痕迹。同样,水垢的生长会随着规则的环空形成而继续,但是新的水垢基质仍然没有矿物。长达10周的实验产生了均匀的椎体骨软化症,而没有明显诱发骨骼畸形。实验表明,在所检查的鱼类中,骨的形成和矿化在很大程度上是独立的过程。因此,矿化不足不一定是在养殖的S. salar中观察到的椎骨结构改变的唯一原因。讨论了观察到的骨形成和矿化的解耦如何有助于更好地诊断,了解和预防养殖的S. salal中与磷缺乏相关的畸形。

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