Parks D A, Williams T K, Beckman J S
Department of Anesthesiology, University of Alabama, Birmingham 35233.
Am J Physiol. 1988 May;254(5 Pt 1):G768-74. doi: 10.1152/ajpgi.1988.254.5.G768.
Oxygen radicals derived from xanthine oxidase (XO) are important mediators of the cellular injury associated with reperfusion of ischemic intestine, stomach, liver, kidney, and pancreas. XO exists in nonischemic tissue predominantly as xanthine dehydrogenase (XDH) and converts to oxygen radical-producing XO with ischemia. Grinding intestine under liquid nitrogen and placing the powder in phosphate buffer (pH 7.0) containing thiol reductants and protease inhibitors adequately preserved total XDH + XO activity and the percentage in the oxidase form (%XO) for 24 h. Total activity in nonischemic intestine ranged from 374 nmol.min-1.g-1 in duodenum to 138 nmol.min-1.g-1 in ileum, while XO activity was approximately 19% of total activity throughout the entire small intestine. The rate of XDH conversion to XO during normothermic ischemia varied only slightly throughout the intestine, increasing 13% per hour to 34, 46, and 61% XO after 1, 2, and 3 h of ischemia, respectively. Our results contrast with previous reports where XDH conversion to XO occurred within 60 s ischemia but are consistent with physiological and morphological evidence of ischemic injury and provide further support for involvement of XO in intestinal injury associated with ischemia.
源自黄嘌呤氧化酶（XO）的氧自由基是与缺血性肠、胃、肝、肾及胰腺再灌注相关的细胞损伤的重要介质。XO在非缺血组织中主要以黄嘌呤脱氢酶（XDH）的形式存在，并在缺血时转化为产生氧自由基的XO。在液氮中研磨肠组织并将粉末置于含有硫醇还原剂和蛋白酶抑制剂的磷酸盐缓冲液（pH 7.0）中，可使总XDH + XO活性及氧化酶形式的百分比（%XO）在24小时内得到充分保存。非缺血肠组织中的总活性范围为十二指肠中的374 nmol·min⁻¹·g⁻¹至回肠中的138 nmol·min⁻¹·g⁻¹，而XO活性在整个小肠中约占总活性的19%。在常温缺血期间，XDH向XO的转化率在整个肠组织中变化很小，缺血1、2和3小时后分别以每小时13%的速度增加至34%、46%和61%的XO。我们的结果与之前报道的XDH在缺血60秒内就转化为XO的情况形成对比，但与缺血性损伤的生理和形态学证据一致，并为XO参与与缺血相关的肠损伤提供了进一步支持。
