Caddell J L
Department of Pediatrics, Thomas Jefferson University, Philadelphia, USA.
Magnes Res. 1995 Sep;8(3):261-70.
This hypothesis states that magnesium and copper (Cu) deficiency as well as high arterial oxygen pressure may contribute to the pathogenesis of retinopathy of prematurity (ROP), a major cause of blindness in very low birthweight preterm infants. Infants at highest risk have severe respiratory distress with hypoxia and require prolonged oxygen supplements. The retina is a multilayer sheet of neural tissue very rich in polyunsaturated fatty acids (PUFAs), oxygen, and mitochondria, with the highest oxygen consumption of all body tissues. Oxygen free radicals which are generated during metabolism cause lipid peroxidation of the PUFA-rich membranes, impairing retinal function. Magnesium and copper deficiencies provide less protection from oxidative injury which damages neurosensory tissue critical for photodetection. Protective antioxidant enzyme activity is reduced in magnesium and copper deficiency. There is some evidence for a raised level of vasoconstrictor thromboxane A2 (TXA2) in respect to vasodilator prostacyclin (PGI2), which would promote vasoconstriction. Deficiency of magnesium and of copper increase synthesis of TXA2 and decreases synthesis of PGI2. Sustained vasoconstriction leads to vascular occlusion, retinal ischaemia, reactive proliferation of retinal vasculature, and the final stages of ROP. Abundant magnesium and copper may protect the retina from developing ROP.
这一假说指出，镁和铜缺乏以及动脉血氧分压升高可能会导致早产儿视网膜病变（ROP）的发病机制，ROP是极低出生体重早产儿失明的主要原因。风险最高的婴儿会出现伴有缺氧的严重呼吸窘迫，需要长时间吸氧。视网膜是一层富含多不饱和脂肪酸（PUFA）、氧气和线粒体的多层神经组织，其耗氧量在所有身体组织中最高。代谢过程中产生的氧自由基会导致富含PUFA的膜发生脂质过氧化，损害视网膜功能。镁和铜缺乏提供的抗氧化损伤保护较少，而抗氧化损伤对光检测至关重要的神经感觉组织有损害。镁和铜缺乏时，保护性抗氧化酶活性降低。有一些证据表明，与血管舒张剂前列环素（PGI2）相比，血管收缩剂血栓素A2（TXA2）水平升高，这会促进血管收缩。镁和铜缺乏会增加TXA2的合成并减少PGI2的合成。持续的血管收缩会导致血管闭塞、视网膜缺血、视网膜血管反应性增殖以及ROP的最终阶段。充足的镁和铜可能会保护视网膜不发生ROP。
