Autoprotection: stimulated tissue repair permits recovery from injury.
Autoprotection: stimulated tissue repair permits recovery from injury.
复制标题
自我保护：刺激组织修复可以从损伤中恢复。
DOI：
10.1002/jbt.2570090304
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
C. Rao
中科院分区：
文献类型：
--
作者：
H. Mehendale;K. Thakore;C. Rao
自我保护是一种现象，通过这种现象，预先暴露于小剂量的化学物质会导致针对随后施用的致死剂量的相同化合物的保护。虽然 CCl4 的自我保护研究最多，但它也适用于其他化学品。最近的研究表明，由于肝微粒体细胞色素 P-450 含量减少而导致正常致死剂量的 CCl4 生物活性降低的普遍观点不能得到肝损伤（例如坏死）的直接终点的支持。这些发现表明，在自我保护机制中，保护剂量刺激的肝细胞分裂和组织愈合过程发挥着关键作用。在保护剂量的刺激下，肝细胞再生和组织修复的增强似乎可以使肝结构和功能及时恢复和恢复。在缺乏保护剂量的情况下，肝细胞分裂严重不足，而且发生得太晚，无法打破损伤恢复和严重损伤进展之间的微妙平衡，有利于恢复。在 CCl4 的代谢和处置不改变的条件下，秋水仙碱抗有丝分裂作用的自我保护作用的废除支持了这一概念。选择性秋水仙碱抗有丝分裂抑制低剂量 CCl4 诱导的肝细胞分裂和组织修复的早期阶段，导致中毒性肝损伤的进展，导致肝衰竭和死亡。研究表明，苯巴比妥预处理会导致低剂量 CCl4 刺激的细胞分裂推迟 24 小时，从而推迟最佳的自身保护。（摘要截断为 250 字）
Autoprotection is a phenomenon whereby prior exposure to a small dose of a chemical results in protection against a subsequently administered lethal dose of the same compound. While CCl4 autoprotection has been studied the most, it has also been demonstrated for other chemicals. Recent studies indicate that the prevailing concept of decreased bioactivation of the normally lethal dose of CCl4 owing to decreased hepatic microsomal cytochrome P-450 content cannot be supported by direct end points of liver injury such as necrosis. These findings suggest a pivotal role for hepatocellular division and tissue healing processes stimulated by the protective dose in the mechanism of autoprotection. Augmentation of hepatocellular regeneration and tissue repair, stimulated by the protective dose, appears to permit timely recovery and restoration of hepatic structure and function. In the absence of the protective dose, hepatocellular division is substantially deficient and it occurs too late to tip the delicate balance between recovery from injury and progression of massive injury in favor of recovery. Abolition of autoprotection by colchicine antimitosis, under conditions where metabolism and disposition of CCl4 are not altered, is supportive of this concept. Selective colchicine antimitotic suppression of the early phase of hepatocellular division and tissue repair induced by a low dose of CCl4 results in progression of toxic liver injury, leading to hepatic failure and mortality. Studies have shown that pretreatment with phenobarbital results in postponed low-dose CCl4-stimulated cell division by 24 hours, which accordingly postpones the optimal autoprotection.(ABSTRACT TRUNCATED AT 250 WORDS)
在四氯化碳诱导肝再生过程中从白蛋白到甲胎蛋白的转录转换以及其他基因转录的变化。
影响因子：
2.9
作者：
Panduro,A;Shalaby,F;Weiner,FR;Biempica,L;Zern,MA;Shafritz,DA
通讯作者：
Shafritz,DA