Kosowski H, Schild L, Kunz D, Halangk W
Department of Surgery, Division of Experimental Surgery, Otto-von-Guericke-Universität Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany.
Biochim Biophys Acta. 1998 Oct 5;1367(1-3):118-26. doi: 10.1016/s0005-2728(98)00143-1.
Mitochondrial energy metabolism was studied in isolated pancreatic acinar cells during anoxia up to 90 min and reoxygenation for 60 min. To identify critical alterations leading to the known postanoxic impairments in structure and function of acinar cells, adenine nucleotide levels and the rates of phosphorylating and non-phosphorylating respiration were determined. ATP levels and the total amount of adenine nucleotides strongly decreased as early as after 30 min of anoxia. The cells partially restored ATP and the total adenine nucleotides within 60 min of reoxygenation. Long-term anoxia caused an increase in the oligomycin-insensitive part of oxygen consumption. The respiratory capacity measured as uncoupled respiration progressively declined to 40% of controls after 90 min of anoxia. Fluorescence measurements showed that flavoproteins and mitochondrial pyridine nucleotides in reoxygenated cells after short-term anoxia were in a more reduced state than in aerobic controls, and were not fully oxidizable by uncoupling. It is concluded that long-term anoxia produces an irreversible loss of respiratory capacity leading to a limited ATP production. This functional impairment and the progressive damage to acinar cells may be relevant for pancreatic injuries such as acute pancreatitis or post-transplantation pancreatitis.
在长达90分钟的缺氧及随后60分钟的复氧过程中，对分离出的胰腺腺泡细胞的线粒体能量代谢进行了研究。为了确定导致腺泡细胞已知的缺氧后结构和功能损伤的关键改变，测定了腺嘌呤核苷酸水平以及磷酸化呼吸和非磷酸化呼吸的速率。早在缺氧30分钟后，ATP水平和腺嘌呤核苷酸总量就大幅下降。在复氧60分钟内，细胞部分恢复了ATP和腺嘌呤核苷酸总量。长期缺氧导致对寡霉素不敏感的耗氧部分增加。以解偶联呼吸衡量的呼吸能力在缺氧90分钟后逐渐降至对照组的40%。荧光测量表明，短期缺氧后复氧细胞中的黄素蛋白和线粒体吡啶核苷酸比需氧对照组处于更还原的状态，且不能通过解偶联完全氧化。得出的结论是，长期缺氧会导致呼吸能力不可逆转的丧失，从而导致ATP生成受限。这种功能损伤以及腺泡细胞的渐进性损伤可能与胰腺炎或移植后胰腺炎等胰腺损伤有关。
