|Abstract: ||鯉魚 (Cyprinus carpio) 消化道組織含有高鋅濃度 (約 300 μg/ g tissue)。當需要鋅時，如缺氧，會釋放鋅作為信號，刺激鯉魚頭腎組織製造新生紅血球。貧血的定義是紅血球的總量減少。根據鯉魚的研究，以苯肼誘導大鼠產生貧血，補充鋅也能刺激大鼠體內紅血球形成。鋅顯然也是一種紅血球生成刺激劑。由於慢性腎病患者缺乏足夠的紅血球生成素之調節，常併發貧血症狀。同時其血漿鋅濃度普遍較低。目前並不清楚腎臟病中貧血與血漿低鋅間是否有相關。本報告以 5/6 腎臟切除大鼠及普通大鼠作為材料，誘導大鼠貧血，再研討貧血與組織中鋅變化之關係。 以動物實驗建立 5/6 腎臟切除大鼠之模型，誘導腎臟病，減少紅血球生成，產生腎性貧血。在實驗第二週，5/6 腎臟切除大鼠之紅血球計數為普通大鼠之85%。另外以 phenylhydrazine (PHZ) 誘導大鼠之貧血，結果顯示，由兩者方式產生之貧血大鼠的 plasma 鋅濃度較低、血球細胞鋅濃度較高，由於實驗中均食用相同的市售飼料，因此血漿鋅濃度的下降及血球鋅濃度的上升，與飲食來源無關，較可能與體內鋅之重新分配 (Zn redistribution) 有關係。 當鯉魚發生嚴重貧血，鋅會作為訊號因子，刺激紅血球生成。然而大鼠是否也有類似的機制，會將體內之鋅移轉至骨髓，以製造新生紅血球，目前並不清楚。為了解大鼠體內各組織之鋅，在鋅之來源過量或不足時，是否會移動，乃分別以普通大鼠及 5/6 腎臟切除大鼠進行實驗。在額外過量補充鋅之時，大鼠軟組織之鋅濃度，並不會因過量補充鋅而有變化；但是會貯存於大腿骨，使其鋅濃度增加。當缺鋅之時，不論是普通大鼠或腎病大鼠，軟組織並不因缺鋅而有明顯變化；然而，大腿骨之鋅濃度皆會大幅下降。由此得知，大鼠的大腿骨是鋅之貯藏庫，可以貯藏鋅，其中的鋅可以被移動，使體內的鋅重新分配，以因應鋅之過量，或不足。當大鼠發生貧血時骨頭之鋅被移至骨髓，以增生紅血球，減緩緊迫。 先前研究指出，添加適量的鋅能刺激 PHZ 所誘導的貧血大鼠，增生紅血球。本報告製成之缺鋅大鼠，在誘導貧血後，缺鋅大鼠血漿中之鋅、血球中之鋅、大腿骨之鋅、骨髓中之新生紅血球以及骨髓間之鋅皆與誘導貧血前，沒有差異。此實驗結果證實，大鼠在貧血後，血漿鋅下降之現象，極有可能是大鼠身上鋅的重組 (redistribution) 而來。大鼠貧血不但會造成血漿鋅之下降，也會造成大腿骨之鋅下降。|
Cyprinus carpio digestive tract tissue contains high Zn concentrations (approximately 300 μg/g tissue). When Zn is needed, such as lack of oxygen, Zn is released as a signal to stimulate the head kidney of the carp to produce new red blood cells (RBC). Anemia is defined as a decrease in the total amount of RBC. In phenylhydrazine (PHZ) induced anemic rats, Zn supplementation also stimulates RBC formation in rats. Due to the lack of adequate regulation of erythropoietin in patients with chronic kidney disease, symptoms of anemia often occur. At the same time, the patient plasma Zn concentration is generally low. It is unclear whether there is a correlation between anemia in kidney disease and low plasma Zn. This article used 5/6-kidney-removal rats and normal rats as material to study the relation between induced anemia and Zn change in rats. Animal models were used to establish the 5/6-kidney-removal rat model to induce kidney disease, and produce renal anemia. In the second week of the experiment, the RBC count of 5/6-kidney-removal rats was 85% of that of normal rats. In addition, PHZ induced anemia in rats. The results showed that anemic rats produced by 5/6-kidney-removal and PHZ treatment had lower plasma Zn concentration and higher blood cell Zn concentration. Because same feed was consumed in the experiment, the plasma Zn concentration decreased and the blood Zn concentration increased in the rats had no relation with dietary sources. It is more likely to be related to Zn redistribution in the rat. When severe anemia occurs in common crap, Zn is used as a signal to stimulate the formation of RBC. However, whether rats have the same mechanism is not clear. In order to understand how the Zn level will change in rats when the Zn source is excessive or deficient, ordinary rats and 5/6-kidney-removal rats were used as material. When excess Zn was supplied, the Zn concentration in most rat tissue does not change. However, it was stored in the bone. When Zn is deficient, the Zn concentration in most rat tissue also does not change. However, the Zn concentration in the bone greatly decreased. Therefore, the bone of the rat is a reservoir of Zn, in which Zn can be moved to redistribute Zn in the body in response to excessive or deficiency of Zn. When there is anemia, Zn in the rat bone is moved to the bone marrow to proliferate RBC to slow down stress. Previous studies indicated that the supplementation of appropriate amount of Zn could stimulate RBC proliferation in PHZ-induced anemic rats. In this report, we produced Zn-deficient rats and subjected the rats to PHZ treatment. We found that in the Zn-deficient rats, before and after PHZ treatment, there were no changes in plasma Zn, blood cells Zn level, bone Zn level and proliferation of RBC. These result confirmed that lowering of plasma Zn in anemic rats is most likely due to the redistribution of Zn in rats. Rat anemia may not only cause a decrease in plasma Zn, but may also cause a decrease in bone Zn.