Bury Nicolas, Grosell Martin
King's College London, School of Health and Life Sciences, Franklin Wilkins Building, 150 Stamford Street, London SE1 9NN, UK.
Comp Biochem Physiol C Toxicol Pharmacol. 2003 Jun;135(2):97-105. doi: 10.1016/s1532-0456(03)00021-8.
Iron is a vital micronutrient for teleost fish, being an integral component of proteins involved in cellular respiration and oxygen transfer. However, in excess iron is toxic, and fish need to balance uptake to prevent deficiency vs. potential toxicity. This review assesses the current physiological and molecular knowledge of the mechanisms of iron acquisition in the teleost fish. It focuses on freshwater teleost fish when assessing the gill as a possible site for iron acquisition, and includes a summary of geochemical processes that govern aquatic iron bioavailability. It focuses on marine teleost fish for assessing the mechanism of intestinal iron uptake. Physiological evidence indicates that iron preferentially crosses the apical membrane of both the gills and intestine in the ferrous (Fe2+) state. Molecular evidence supports this, demonstrating the presence of homologues in fish to the large Slc 11a family of evolutionary conserved proteins linked to Fe2+ transport. This symporter is probably linked to a reductase, which reduces either ferric (Fe3+) or organic complexed iron to Fe2+ prior to uptake.
铁是硬骨鱼至关重要的微量营养素,是参与细胞呼吸和氧气传递的蛋白质的重要组成部分。然而,铁过量是有毒的,鱼类需要平衡铁的摄取量,以防止缺铁和潜在的毒性。本综述评估了目前关于硬骨鱼铁获取机制的生理和分子知识。在评估鳃作为铁获取的可能部位时,重点关注淡水硬骨鱼,并总结了控制水生铁生物有效性的地球化学过程。在评估肠道铁摄取机制时,重点关注海洋硬骨鱼。生理学证据表明,铁优先以亚铁(Fe2+)状态穿过鳃和肠道的顶端膜。分子证据支持这一点,证明鱼类中存在与Fe2+转运相关的进化保守的大Slc 11a蛋白家族的同源物。这种协同转运蛋白可能与一种还原酶相关联,该还原酶在摄取之前将三价铁(Fe3+)或有机络合铁还原为Fe2+。