Martin Keith R
Department of Nutritional Sciences, The Pennsylvania State University, 126 Henderson Building South, University Park, PA 16802, USA.
Exp Biol Med (Maywood). 2006 Feb;231(2):117-29. doi: 10.1177/153537020623100201.
Apoptosis, a form of programmed cell death, is a pivotal defense against the occurrence of cancer and is essential to metazoans in maintaining tissue homeostasis. Apoptosis exhibits a distinctive phenotype and involves elimination of potentially deleterious cells. Many diseases have been associated with aberrantly regulated apoptotic cell death, ultimately leading to inhibition of apoptosis and propagation of diseases such as cancer. Elucidation of the critical events associated with carcinogenesis provides the opportunity for dietary intervention to prevent cancer development through induction of apoptosis, particularly by bioactive agents or functional foods. Diet is a significant environmental factor in the overall cancer process and can exacerbate or interfere with carcinogenesis. Apoptosis occurs primarily through two well-recognized pathways in cells, including the intrinsic, or mitochondrial-mediated, effector mechanism and the extrinsic, or death receptor-mediated, effector mechanism. In addition to diet's effects on protein expression and function, evidence is also accumulating that a large number of dietary food components can exert effects on the human genome, either directly or indirectly, to modulate gene expression. In fact, many diet-related genes are involved in carcinogenesis as well as apoptosis, and thus are ultimately molecular targets for dietary chemoprevention. There are multiple steps within pathways in which dietary components can alter gene expression and phenotypes of cells and thus influence cancer outcomes (nutritional transcriptomic effect). Thus, apoptosis is an emerging therapeutic target of bioactive agents of diet. In this review, the process of apoptosis is discussed and the potential mechanistic interaction of bioactive agents, as components of functional foods, is explored within the context of apoptosis.
细胞凋亡是一种程序性细胞死亡形式，是抵御癌症发生的关键防御机制，对于后生动物维持组织稳态至关重要。细胞凋亡表现出独特的表型，涉及清除潜在有害细胞。许多疾病都与凋亡性细胞死亡的异常调节有关，最终导致细胞凋亡受抑制，进而引发癌症等疾病的扩散。阐明与致癌作用相关的关键事件，为通过诱导细胞凋亡进行饮食干预以预防癌症发展提供了机会，特别是通过生物活性剂或功能性食品来实现。饮食是整体癌症进程中的一个重要环境因素，可加剧或干扰致癌作用。细胞凋亡主要通过细胞内两条广为人知的途径发生，包括内在的或线粒体介导的效应机制以及外在的或死亡受体介导的效应机制。除了饮食对蛋白质表达和功能的影响外，越来越多的证据表明，大量的膳食成分可直接或间接对人类基因组产生影响，从而调节基因表达。事实上，许多与饮食相关的基因都参与致癌作用和细胞凋亡，因此最终成为饮食化学预防的分子靶点。在这些途径中有多个步骤，膳食成分可在这些步骤中改变基因表达和细胞表型，进而影响癌症结局（营养转录组效应）。因此，细胞凋亡是饮食生物活性剂一个新出现的治疗靶点。在本综述中，我们讨论了细胞凋亡过程，并在细胞凋亡的背景下探讨了作为功能性食品成分的生物活性剂的潜在机制相互作用。
