人乳头瘤病毒 (HPV) 对癌症的影响是显着的，但并非排他性的，因为致癌涉及复杂的机制，尤其是氧化应激。氧化应激和 HPV 可以独立导致基因组不稳定和 DNA 损伤，从而促进肿瘤发生。氧化应激诱导的 DNA 损伤，尤其是双链断裂，有助于 HPV 整合到宿主基因组中，并促进两种病毒蛋白 E6 和 E7 的过度表达。生活方式因素，包括饮食、吸烟、饮酒和心理压力，以及遗传和表观遗传修饰以及病毒癌蛋白可能会影响氧化应激，从而影响 HPV 相关癌症的进展。这篇综述强调了氧化诱导 HPV 介导的致癌作用的各种机制，包括线粒体形态和功能的改变导致 ROS 水平升高、超氧化物歧化酶 (SOD)、谷胱甘肽 (GSH) 和谷胱甘肽过氧化物酶 (GPx) 等抗氧化酶的调节、诱导慢性炎症环境的影响，以及特定细胞信号传导途径的激活，如磷酸肌醇 3 激酶、蛋白激酶 B、哺乳动物雷帕霉素靶点 (PI3K/AKT/mTOR) 和细胞外信号调节激酶 (ERK) 信号传导途径。该研究强调了理解和控制氧化应激在预防和治疗癌症中的重要性。我们建议，纳入膳食抗氧化剂并通过涉及 ROS 的机制靶向癌细胞可能是减轻氧化应激对 HPV 相关恶性肿瘤影响的潜在干预措施。© 2024。作者。

The contribution of the human papillomavirus (HPV) to cancer is significant but not exclusive, as carcinogenesis involves complex mechanisms, notably oxidative stress. Oxidative stress and HPV can independently cause genome instability and DNA damage, contributing to tumorigenesis. Oxidative stress-induced DNA damage, especially double-strand breaks, aids in the integration of HPV into the host genome and promotes the overexpression of two viral proteins, E6 and E7. Lifestyle factors, including diet, smoking, alcohol, and psychological stress, along with genetic and epigenetic modifications, and viral oncoproteins may influence oxidative stress, impacting the progression of HPV-related cancers. This review highlights various mechanisms in oxidative-induced HPV-mediated carcinogenesis, including altered mitochondrial morphology and function leading to elevated ROS levels, modulation of antioxidant enzymes like Superoxide Dismutase (SOD), Glutathione (GSH), and Glutathione Peroxidase (GPx), induction of chronic inflammatory environments, and activation of specific cell signaling pathways like the Phosphoinositide 3-kinase, Protein kinase B, Mammalian target of rapamycin (PI3K/AKT/mTOR) and the Extracellular signal-regulated kinase (ERK) signaling pathway. The study highlights the significance of comprehending and controlling oxidative stress in preventing and treating cancer. We suggested that incorporating dietary antioxidants and targeting cancer cells through mechanisms involving ROS could be potential interventions to mitigate the impact of oxidative stress on HPV-related malignancies.© 2024. The Author(s).