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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Remediation Sign in to save

Cancer Metabolism: The Role of ROS in DNA Damage and Induction of Apoptosis in Cancer Cells

Metabolites 2023 229 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 70 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Yongxia Zhao, Yongxia Zhao, Xiaochun Ye, Zhifeng Xiong, Zhifeng Xiong, María‐Aránzazu Martínez Awais Ihsan, Irma Arés, Marta Martínez, Bernardo López-Torres, María‐Rosa Martínez‐Larrañaga, Arturo Anadón, Xu Wang, María‐Aránzazu Martínez

Summary

This review explores how reactive oxygen species (ROS) -- harmful molecules produced during abnormal cell metabolism -- can damage DNA and trigger cancer cell death, making ROS a potential target for cancer treatment. While not directly about microplastics, this is relevant because microplastic exposure is known to increase ROS production in human cells, which could contribute to DNA damage over time.

Cancer is a huge challenge for people worldwide. High reactive oxygen species (ROS) levels are a recognized hallmark of cancer and an important aspect of cancer treatment research. Abnormally elevated ROS levels are often attributable to alterations in cellular metabolic activities and increased oxidative stress, which affects both the development and maintenance of cancer. Moderately high levels of ROS are beneficial to maintain tumor cell genesis and development, while toxic levels of ROS have been shown to be an important force in destroying cancer cells. ROS has become an important anticancer target based on the proapoptotic effect of toxic levels of ROS. Therefore, this review summarizes the role of increased ROS in DNA damage and the apoptosis of cancer cells caused by changes in cancer cell metabolism, as well as various anticancer therapies targeting ROS generation, in order to provide references for cancer therapies based on ROS generation.

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