25 June 2024 | Hari Krishnan Krishnamurthy, Imbaasree Rajavelu, Michelle Pereira, Vasanth Jayaraman, Karthik Krishna, Tianhao Wang, Kang Bei and John J. Rajasekaran
This review explores the genetic factors influencing oxidative stress, focusing on prooxidant and antioxidant genes. Oxidative stress arises from an imbalance between oxidants and antioxidants, leading to cellular damage. Prooxidant genes, such as XDH, CYBA, CYP1A1, PTGS2, NOS, and MAO, contribute to the production of reactive oxygen species (ROS), while antioxidant genes like SOD, CAT, GPX, GSS, GLUL, GSR, GSTM1, GSTM5, GSTP1, TXN, and HMOX1 help neutralize these species. Genetic variations in these genes can affect their function and efficiency, increasing the risk of oxidative stress. Understanding these genetic influences can lead to personalized medicine approaches that tailor healthcare to individual genetic profiles. The review highlights key SNPs in these genes and their associations with oxidative stress-related diseases, such as cancer, diabetes, atherosclerosis, and cardiovascular diseases. It also discusses the role of signaling pathways like Nrf2/ARE, NF-κB, PI3K/AKT, and others in managing oxidative stress. The study emphasizes the importance of genetic assessment and biological markers in improving treatment strategies and mitigating oxidative damage. Overall, the review underscores the significance of genetic insights in understanding and managing oxidative stress.This review explores the genetic factors influencing oxidative stress, focusing on prooxidant and antioxidant genes. Oxidative stress arises from an imbalance between oxidants and antioxidants, leading to cellular damage. Prooxidant genes, such as XDH, CYBA, CYP1A1, PTGS2, NOS, and MAO, contribute to the production of reactive oxygen species (ROS), while antioxidant genes like SOD, CAT, GPX, GSS, GLUL, GSR, GSTM1, GSTM5, GSTP1, TXN, and HMOX1 help neutralize these species. Genetic variations in these genes can affect their function and efficiency, increasing the risk of oxidative stress. Understanding these genetic influences can lead to personalized medicine approaches that tailor healthcare to individual genetic profiles. The review highlights key SNPs in these genes and their associations with oxidative stress-related diseases, such as cancer, diabetes, atherosclerosis, and cardiovascular diseases. It also discusses the role of signaling pathways like Nrf2/ARE, NF-κB, PI3K/AKT, and others in managing oxidative stress. The study emphasizes the importance of genetic assessment and biological markers in improving treatment strategies and mitigating oxidative damage. Overall, the review underscores the significance of genetic insights in understanding and managing oxidative stress.