Ion regulation, cell injury and carcinogenesis.

Ion regulation, cell injury and carcinogenesis.
复制标题

离子调节、细胞损伤和致癌。

DOI:
10.1093/carcin/8.8.1027
复制
发表时间:
1987
期刊:
影响因子:
4.7
通讯作者:
Berezesky,IK
Berezesky,IK
中科院分区:
医学2区
文献类型:
--
作者:
Trump,BF;Berezesky,IK

文献摘要

被引文献

相似文献

这篇评论涉及离子调节、毒性和致癌作用,总结了目前的进展,考虑了新的研究发现,并扩展了我们自己之前关于离子调节、细胞损伤和分化的作用的假设(1-4)。近年来,人们越来越清楚地认识到,细胞分裂、细胞死亡、细胞分化与癌变之间存在着密切的关系。几乎所有完全致癌物在致癌剂量下都具有急性毒性,慢性毒性通常在随后的瘤变评估期间持续存在;例如,皮肤损伤已被确定为一种启动子,流行病学数据有力地表明,烟草烟雾的主要影响是慢性的、反复的伤害性损伤,并且越来越多的实例表明,NT a、糖精和无铅汽油等非致突变性、非致裂性化合物会产生初始和慢性毒性,最终导致致癌。因此,假设在这几种看似不同的状态中存在一个或多个共同因素是合理的。在本文中,我们将提出一个假设,即细胞内电离钙([Ca],*)的解除管制构成了这样一个因素。
This commentary concerns ion regulation, toxicity and carcinogenesis, summarizes current advances, considers new research findings and extends our own previous hypothesis on the role of ion regulation, cell injury and differentiation (1—4). It has become increasingly evident in recent years diat there is an intimate relationship between the cellular events involved in cell division, cell death, cell differentiation and carcinogenesis. Virtually all complete carcinogens are acutely toxic at carcinogenic doses and chronic toxicity typically continues during the evaluation of the subsequent neoplasia; for example, wounding in the skin is well established as a promoter, epidemiologic data strongly indicate that the major effect of tobacco smoke is chronic, repeated injurious insults, and there are increasing instances where non-mutagenic, non-clastogenic compounds such as NT A, saccharin and unleaded gasoline that produce initial and chronic toxicity result ultimately in carcinogenesis. It is, therefore, reasonable to hypodiesize mat a common factor or factors exist in these several seemingly disparate states. In this paper, we will develop the hypothesis that deregulation of intracellular ionized calcium ([Ca],*) constitutes such a factor.