English  |  正體中文  |  简体中文  |  Items with full text/Total items : 43312/67235
Visitors : 2079402      Online Users : 4
RC Version 5.0 © Powered By DSPACE, MIT. Enhanced by NTU/NCHU Library IR team.

Please use this identifier to cite or link to this item: http://nchuir.lib.nchu.edu.tw/handle/309270000/152374

標題: 點帶石斑魚面臨海洋酸化時的生理反應
Physiological responses to ocean acidification in orange-spotted grouper (Epinephelus coioides)
作者: 洪國凱
Hong, Guo-Kai
Contributors: 湯政豪
Cheng-Hao Tang
生命科學系所
關鍵字: 點帶石斑魚;海洋酸化;逆境反應
orange-spotted grouper;ocean acidification;stress responses
日期: 2013
Issue Date: 2013-11-07 13:23:44 (UTC+8)
Publisher: 生命科學系所
摘要: 根據對海洋酸化的研究瞭解,現今海水平均的pH值約為8.1,預測於2100年時全球海水的pH值將下降至7.7,於2300年時海水的pH值下降至7.4。暴露在預測的酸化程度刺激下,研究海洋生物會產生如何的生理反應,對於預測未來海洋酸化的影響是很重要的。本研究將珊瑚礁魚類點帶石斑魚,曝露於兩種不同程度的海洋酸化下(pH 7.7 和pH 7.4),實驗期間為一週,研究其逆境刺激反應、酸鹼調節機制以及能量代謝等生理反應。由實驗結果顯示,暴露在酸化環境下,點帶石斑魚鰓上HSP70蛋白質表現量及血液葡萄糖含量皆有顯著性的提升。推測海洋酸化將會對點帶石斑魚造成了逆境刺激反應,誘導HSP70表現量上升及提高血液葡萄糖含量以抵抗海洋酸化的影響。接著由探討鰓上酸鹼調節相關的蛋白質,包括Na+/K+-ATPase (NKA), V-type H+-ATPases (VHA) 和 cytosolic carbonic anhydrase (CAc),並配合血液滲透壓以及血液酸鹼平衡相關參數 (pCO2, HCO3- and pH )。由結果顯示暴露在酸化環境下,NKA, HA及CAc的蛋白質表現量或是活性皆有顯著性提升,也觀察到血液滲透壓及血液pH值能維持在正常範圍內。推測海洋酸化影響下,點帶石斑魚能藉由提升鰓上NKA,VHA以及CAc等蛋白質表現量及活性,執行酸鹼調節功能,以維持血液滲透壓及血液pH值的恆定。此外,探討海洋酸化對能量代謝的影響。由結果發現暴露在酸化環境下,鰓上肝糖含量有累積的情形發生,且pyruvate kinase (PK)及cytochrome c oxidase (COX)的mRNA表現量皆有顯著性的提升。推測海洋酸化影響下,點帶石斑的鰓上必須累積肝糖並製造能量,以提供鰓去面對海洋酸化所帶來的影響。而肝臟的肝糖含量以及肌肉的myosin 和myostatin mRNA表現量皆無受到酸化所影響,推測在整體能量儲存及個體成長上,並不受海洋酸化所影響。本篇實驗是第一篇藉由分子層級角度下,探討珊瑚礁魚類在面對海洋酸化刺激下所誘發的多種不同的生理調節機制。
According to ocean acidification researches, the pH of seawater is about 8.1 nowadays. It is estimated the pH will decrease to 7.7 in 2100, and 7.4 in 2300. Thus it is important to investigate the physiological responses for prediction of the implications of ocean acidification on marine organisms. In this regard, a reef-associated species, orange-spotted grouper (Epinephelus coioides), was used to explore the influence of two levels (pH 7.7 and pH7.4) of ocean acidification on the physiological responses at various aspects, including stress response, acid-base regulation, and energy metabolism. In stress response, both the expression of heat shock protein 70 (HSP70) and plasma glucose levels elevated significantly in response to hypercapnia. It was suggested induction of stress responses could cope with the challenge of ocean acidification. By using acid-base regulation related proteins including Na+/K+-ATPase (NKA), H+-ATPases (VHA), and cytosolic carbonic anhydrase (CAc), in addition to plasma osmolality and blood acid-base parameter (pCO2, [HCO3-] and pH ), the results showed that NKA,VHA and CAc were up-regulated significantly in response to hypercapnia, but plasma osmolality and blood pH were unaffected. It was suggested that grouper will elevate protein expression and activity of NKA,VHA and CAc to perform acid-base regulation and maintained within a homeostatic range of plasma osmolality and blood pH. Furthermore, in energy metabolism of ocean acidification effect, the gill glycogen content, mRNA expression of pyruvate kinase (PK) and cytochrome c oxidase (COX) are up-regulated significantly in response to hypercapnia. It suggests that orange-spotted grouper (E. coioides) have to accumulate glycogen and produce energy in gill in order to against influence of ocean acidification. However, the liver glycogen contents and mRNA expression of muscle myosin and myostatin were not affected by ocean acidification. This integrative study investigated multiple physiological responses in a marine teleost to ocean acidification. Our study provided evidences that E. coioides consumed more energy to conduct stress response and acid-base regulatory mechanism to adapt and survive in increasingly serious ocean acidification.
Appears in Collections:[依資料類型分類] 碩博士論文

Files in This Item:

File SizeFormat
index.html0KbHTML149View/Open


 


學術資源

著作權聲明

本網站為收錄中興大學學術著作及學術產出,已積極向著作權人取得全文授權,並盡力防止侵害著作權人之權益。如仍發現本網站之數位內容有侵害著作權人權益情事者,請權利人通知本網站維護人員,將盡速為您處理。

本網站之數位內容為國立中興大學所收錄之機構典藏,無償提供學術研究與公眾教育等公益性使用。

聯絡網站維護人員:wyhuang@nchu.edu.tw,04-22840290 # 412。

DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU/NCHU Library IR team Copyright ©   - Feedback