Rauen U, Elling B, de Groot H
Institut für Physiologische Chemie, Universitätsklinikum, Essen, Germany.
Free Radic Biol Med. 1997;23(3):392-400. doi: 10.1016/s0891-5849(96)00618-1.
When cultured liver endothelial cells were incubated in cold University of Wisconsin (UW) solution under hypoxic conditions, 3 +/- 2% of cells had lost viability after 25 h. Simulating reperfusion by returning the cells to normal cell culture conditions increased the injury to 30 +/- 11% after 3 h of recultivation. An injury of similar time course was observed after cold normoxic incubation in UW solution when the loss of viability increased from 20 +/- 5% after the cold incubation to 60 +/- 8% during a 3 h recultivation period. The loss of viability during recultivation was decreased by hypoxia, by the addition of 5,5-dimethyl-1-pyrroline N-oxide or of dimethyl sulfoxide to the cell culture medium, or by preincubating the cells with deferoxamine. The injury was accompanied by lipid peroxidation and was dependent on the period of cold incubation in UW solution. These results suggest the occurrence of a cold-preservation-induced "recultivation injury" mediated by reactive oxygen species. This cold-preservation-induced injury--occurring independently of hypoxia/reoxygenation--is likely to constitute an additional component of reperfusion injury after cold preservation of the liver.
当在缺氧条件下将培养的肝内皮细胞置于冷的威斯康星大学（UW）溶液中孵育时，25小时后有3±2%的细胞失去活力。通过将细胞恢复到正常细胞培养条件来模拟再灌注，在再培养3小时后，损伤增加到30±11%。当在UW溶液中进行冷常氧孵育时，观察到类似时间进程的损伤，活力丧失从冷孵育后的20±5%增加到再培养3小时期间的60±8%。再培养期间的活力丧失可通过缺氧、向细胞培养基中添加5,5-二甲基-1-吡咯啉N-氧化物或二甲基亚砜，或用去铁胺预孵育细胞而降低。这种损伤伴有脂质过氧化，并且取决于在UW溶液中的冷孵育时间。这些结果表明存在由活性氧介导的冷保存诱导的“再培养损伤”。这种独立于缺氧/复氧而发生的冷保存诱导的损伤可能构成肝脏冷保存后再灌注损伤的一个额外组成部分。
