正常组织的治疗耐药性和毒性是化疗和放疗疗效的主要问题。耐药性是大多数与癌症相关的死亡病例的原因。此外，它们的副作用会降低幸存患者的生活质量。增强肿瘤对治疗的反应和减轻毒性作用仍然是未解决的挑战。有趣的主题之一是使用低毒性药物来保护正常组织和/或使癌症对化疗/放疗敏感。褪黑激素是一种天然的体内激素，被称为多任务分子。尽管它具有抗氧化特性，但大量实验发现褪黑激素具有有趣的作用，可以提高化疗/放射治疗的疗效。褪黑激素可以通过多种机制、细胞如免疫系统、细胞周期和死亡途径的调节、肿瘤抑制基因以及通过抑制一些耐药介质来增强抗癌治疗效果。然而，褪黑激素可以通过抑制正常细胞和组织中的炎症、纤维化和大量氧化应激来保护正常组织。在这篇综述中，我们将讨论褪黑激素对肿瘤和正常组织的独特影响。我们回顾了褪黑激素如何增强肿瘤的放射/化学敏感性，同时保护肺、心脏、胃肠系统、生殖系统、大脑、肝脏和肾脏等正常组织。版权所有© Bentham Science Publishers；如有任何疑问，请发送电子邮件至 epub@benthamscience.net。

Resistance to therapy and the toxicity of normal tissue are the major problems for efficacy associated with chemotherapy and radiotherapy. Drug resistance is responsible for most cases of mortality associated with cancer. Furthermore, their side effects can decrease the quality of life for surviving patients. An enhancement in the tumor response to therapy and alleviation of toxic effects remain unsolved challenges. One of the interesting topics is the administration of agents with low toxicity to protect normal tissues and/or sensitize cancers to chemo/radiotherapy. Melatonin is a natural body hormone that is known as a multitasking molecule. Although it has antioxidant properties, a large number of experiments have uncovered interesting effects of melatonin that can increase the therapeutic efficacy of chemo/radiation therapy. Melatonin can enhance anticancer therapy efficacy through various mechanisms, cells such as the immune system, and modulation of cell cycle and death pathways, tumor suppressor genes, and also through suppression of some drug resistance mediators. However, melatonin may protect normal tissues through the suppression of inflammation, fibrosis, and massive oxidative stress in normal cells and tissues. In this review, we will discuss the distinct effects of melatonin on both tumors and normal tissues. We review how melatonin may enhance radio/chemosensitivity of tumors while protecting normal tissues such as the lung, heart, gastrointestinal system, reproductive system, brain, liver, and kidney.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.