BRCA1 protein dose-dependent risk for embryonic oxidative DNA damage, embryopathies and neurodevelopmental disorders with and without ethanol exposure

Drake, Danielle M.; Afsharian, Kian; Or, Benjamin; Shapiro, Aaron M.; Lai, Michelle L.; Miller, Lutfiya; Wells, Peter G.

doi:10.1016/j.redox.2024.103070

Cited by 2 publications

(1 citation statement)

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“…The main DNA base damage caused by ROS is 8-oxoguanine (8-oxoG), which is repaired by oxoguanine glycosylase 1 (OGG1) [317]. BRCA1 transcriptionally activates OGG1 upon generation of 8-oxoG for its repair [316,318]. Inactivation of BRCA1 causes high levels of oxidative stress with increased production of superoxide anions and H 2 O 2 and increases cell sensitivity to oxidative stress, reducing cell viability [319].…”

Section: Brca1 and Oxidative Stressmentioning

confidence: 99%

Oxidative Stress in Breast Cancer: A Biochemical Map of Reactive Oxygen Species Production

Bel’skaya,

Dyachenko

2024

CIMB

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This review systematizes information about the metabolic features of breast cancer directly related to oxidative stress. It has been shown those redox changes occur at all levels and affect many regulatory systems in the human body. The features of the biochemical processes occurring in breast cancer are described, ranging from nonspecific, at first glance, and strictly biochemical to hormone-induced reactions, genetic and epigenetic regulation, which allows for a broader and deeper understanding of the principles of oncogenesis, as well as maintaining the viability of cancer cells in the mammary gland. Specific pathways of the activation of oxidative stress have been studied as a response to the overproduction of stress hormones and estrogens, and specific ways to reduce its negative impact have been described. The diversity of participants that trigger redox reactions from different sides is considered more fully: glycolytic activity in breast cancer, and the nature of consumption of amino acids and metals. The role of metals in oxidative stress is discussed in detail. They can act as both co-factors and direct participants in oxidative stress, since they are either a trigger mechanism for lipid peroxidation or capable of activating signaling pathways that affect tumorigenesis. Special attention has been paid to the genetic and epigenetic regulation of breast tumors. A complex cascade of mechanisms of epigenetic regulation is explained, which made it possible to reconsider the existing opinion about the triggers and pathways for launching the oncological process, the survival of cancer cells and their ability to localize.

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