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REVIEW ARTICLE
Year : 2014  |  Volume : 10  |  Issue : 4  |  Page : 811-818

Reactive oxygen species as mediator of tumor radiosensitivity


Division of Life Sciences, Research Centre, Nehru Gram Bharati University, Allahabad, Uttar Pradesh, India

Correspondence Address:
Kaushala Prasad Mishra
Division of Life Sciences, Research Centre, Nehru Gram Bharati University, Allahabad - 211 002, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.146073

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In normal functioning of the cell, there is a balance between generation and neutralization of reactive oxygen species (ROS) by endogenous cellular defense machinery. Low levels of ROS inside the cells are required for normal functioning of the cell, which regulate signaling mechanisms involved in mitosis and apoptosis; excess of ROS production may cause oxidative stress leading to damage in vital cellular molecules, namely cytosolic lipids, proteins, and DNA. In the situation of intracellular redox imbalance, molecules of cells are altered by ROS leading to pathogenic state. It is to be noted that ROS is not only known to be involved in tumor induction and progression processes but also enhances tumor cell radiosensitivity. The level of ROS-mediated oxidative stress is linked to cellular radiosensitivity. In general, cancer cells exhibit high levels of ROS, which forms a target for selectively killing them by radiation. In this paper, we have reviewed how oxidative stress determines the radiosensitivity of tumor cells involving ROS in the mechanism of radiation induced tumor cell killing. It is suggested that radiation-induced ROS play a key role in the mechanism of tumor cell killing by altering the signaling network and triggering of apoptosis. Furthermore, it is pointed out that combined use of plant-derived antioxidants and radiation enhance overproduction of ROS in tumor cells leading to enhanced radiosensitivity, which may find practical applications in clinic.

Abstract in Chinese

活性氧粒子作为肿瘤辐射敏感性的介质 摘要 在正常运作的细胞中,活性氧粒子(ROS)的生成和中和是由内源性细胞防御机制来达到平衡的。在细胞的正常运作中,低水平的ROS是所需的,它参与调节有丝分裂和细胞凋亡的信号传导机制;过量的ROS可引起氧化应激导致细胞分子的损伤,即细胞内脂质,蛋白质和DNA的损伤。在细胞内氧化还原失衡的情况下,ROS将改变分子细胞导致致病状态。值得注意的是,ROS不仅是参与肿瘤的诱导和进展过程,而且提高了肿瘤细胞的放射敏感性。ROS介导的氧化应激的水平与细胞的放射敏感性有关。一般来说,癌细胞表现出高水平的ROS,因此可以选择放射治疗来杀伤它们。在本文中,我们回顾了氧化应激决定肿瘤细胞的辐射敏感性,包括ROS在诱导辐射杀伤肿瘤细胞中的机制。这表明辐射诱导的ROS在肿瘤细胞通过改变信令网和触发细胞凋亡杀伤机制中发挥重要的作用。此外,还有一点也被指出,即联合使用植物来源的抗氧化剂和辐射增强生产过剩的ROS将导致肿瘤细胞的放射增敏,这可见于临床实际应用中。 关键词:抗氧化剂,氧化应激,辐射,活性氧,肿瘤的放射敏感性,肿瘤毒性



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