Related Experiment Videos
Role of reactive oxygen species in apoptosis: implications for cancer therapy
J M Matés1, F M Sánchez-Jiménez
1Department of Molecular Biology and Biochemistry, Sciences Faculty, University of Málaga, Campus de Teatinos, Málaga, Spain. jmates@uma.es
Abstract:
Reactive oxygen species are widely generated in biological systems. Consequently humans have evolved antioxidant defence systems that limit their production. Intracellular production of active oxygen species such as *OH, O2- and H2O2 is associated with the arrest of cell proliferation. Similarly, generation of oxidative stress in response to various external stimuli has been implicated in the activation of transcription factors and to the triggering of apoptosis. Here we review how free radicals induce DNA sequence changes in the form of mutations. deletions, gene amplification and rearrangements. These alterations may result in the initiation of apoptosis signalling leading to cell death, or to the activation of several proto-oncogenes and or the inactivation of some tumour suppressor genes. The regulation of gene expression by means of oxidants, antioxidants and the redox state remains as a promising therapeutic approach. Several anticarcinogenic agents have been shown to inhibit reactive oxygen species production and oxidative DNA damage, inhibiting tumour promotion. In addition, recombinant vectors expressing radical-scavenging enzymes reduce apoptosis. In conclusion, oxidative stress has been implicated in both apoptosis and the pathogenesis of cancer providing contrived support for two notions: free radical reactions may be increased in malignant cells and oxidant scavenging systems may be useful in cancer therapy.
Insights
Reactive oxygen species (ROS) cause DNA damage, mutations, and cell death, impacting cancer development. Antioxidant therapies targeting ROS show promise for cancer treatment and preventing tumor promotion.
Area of Science:
- Biochemistry and Molecular Biology
- Genetics and Genomics
- Cancer Research
Background:
- Reactive oxygen species (ROS) are integral to biological systems, necessitating evolved antioxidant defenses.
- Intracellular ROS production is linked to cell proliferation arrest, oxidative stress, transcription factor activation, and apoptosis.
- Oxidative stress influences cellular processes, including DNA damage and gene expression regulation.
Purpose of the Study:
- To review the mechanisms by which free radicals induce DNA alterations.
- To explore the role of oxidative stress in apoptosis and cancer pathogenesis.
- To discuss the therapeutic potential of targeting ROS and oxidative stress in cancer.
Main Methods:
- Literature review of studies on reactive oxygen species, oxidative stress, and DNA damage.
- Analysis of the impact of free radicals on DNA sequences, including mutations, deletions, gene amplification, and rearrangements.
- Examination of the role of oxidants, antioxidants, and redox state in gene expression regulation.
Main Results:
- Free radicals induce DNA sequence changes, potentially leading to apoptosis or alterations in proto-oncogenes and tumor suppressor genes.
- Oxidative DNA damage is implicated in tumor promotion.
- Recombinant vectors expressing radical-scavenging enzymes can reduce apoptosis.
Conclusions:
- Oxidative stress plays a dual role in apoptosis and cancer pathogenesis.
- Malignant cells may exhibit increased free radical reactions.
- Antioxidant and oxidant-scavenging systems represent a promising therapeutic strategy for cancer treatment.