Di Carlo Emma, Sorrentino Carlo
Department of Medicine and Sciences of Aging, "G. d'Annunzio" University of Chieti-Pescara, 66100 Chieti, Italy.
Anatomic Pathology and Immuno-Oncology Unit, Center for Advanced Studies and Technology (CAST), "G. d'Annunzio" University of Chieti-Pescara, 66100 Chieti, Italy.
Antioxidants (Basel). 2024 Sep 13;13(9):1109. doi: 10.3390/antiox13091109.
Oxidative stress is the result of the imbalance between reactive oxygen and nitrogen species (RONS), which are produced by several endogenous and exogenous processes, and antioxidant defenses consisting of exogenous and endogenous molecules that protect biological systems from free radical toxicity. Oxidative stress is a major factor in the aging process, contributing to the accumulation of cellular damage over time. Oxidative damage to cellular biomolecules, leads to DNA alterations, lipid peroxidation, protein oxidation, and mitochondrial dysfunction resulting in cellular senescence, immune system and tissue dysfunctions, and increased susceptibility to age-related pathologies, such as inflammatory disorders, cardiovascular and neurodegenerative diseases, diabetes, and cancer. Oxidative stress-driven DNA damage and mutations, or methylation and histone modification, which alter gene expression, are key determinants of tumor initiation, angiogenesis, metastasis, and therapy resistance. Accumulation of genetic and epigenetic damage, to which oxidative stress contributes, eventually leads to unrestrained cell proliferation, the inhibition of cell differentiation, and the evasion of cell death, providing favorable conditions for tumorigenesis. Colorectal, breast, lung, prostate, and skin cancers are the most frequent aging-associated malignancies, and oxidative stress is implicated in their pathogenesis and biological behavior. Our aim is to shed light on the molecular and cellular mechanisms that link oxidative stress, aging, and cancers, highlighting the impact of both RONS and antioxidants, provided by diet and exercise, on cellular senescence, immunity, and development of an antitumor response. The dual role of ROS as physiological regulators of cell signaling responsible for cell damage and diseases, as well as its use for anti-tumor therapeutic purposes, will also be discussed. Managing oxidative stress is crucial for promoting healthy aging and reducing the risk of age-related tumors.
氧化应激是活性氧和氮物种(RONS)与抗氧化防御之间失衡的结果。RONS由多种内源性和外源性过程产生,而抗氧化防御则由外源性和内源性分子组成,这些分子可保护生物系统免受自由基毒性的影响。氧化应激是衰老过程中的一个主要因素,随着时间的推移会导致细胞损伤的积累。细胞生物分子的氧化损伤会导致DNA改变、脂质过氧化、蛋白质氧化和线粒体功能障碍,从而导致细胞衰老、免疫系统和组织功能障碍,并增加对与年龄相关疾病的易感性,如炎症性疾病、心血管疾病和神经退行性疾病、糖尿病和癌症。氧化应激驱动的DNA损伤和突变,或甲基化和组蛋白修饰,会改变基因表达,是肿瘤发生、血管生成、转移和治疗耐药性的关键决定因素。氧化应激促成的遗传和表观遗传损伤的积累最终导致细胞不受控制的增殖、细胞分化的抑制和细胞死亡的逃避,为肿瘤发生提供了有利条件。结直肠癌、乳腺癌、肺癌、前列腺癌和皮肤癌是最常见的与衰老相关的恶性肿瘤,氧化应激与它们的发病机制和生物学行为有关。我们的目的是阐明将氧化应激、衰老和癌症联系起来的分子和细胞机制,强调饮食和运动提供的RONS和抗氧化剂对细胞衰老、免疫和抗肿瘤反应发展的影响。还将讨论ROS作为负责细胞损伤和疾病的细胞信号生理调节因子的双重作用,以及其用于抗肿瘤治疗目的的情况。控制氧化应激对于促进健康衰老和降低与年龄相关肿瘤的风险至关重要。