Your body constantly reacts with oxygen as you breathe and your cells produce energy. As a consequence of this activity, highly reactive molecules are produced within our cells known as free radicals and oxidative stress occurs.
Oxidative stress can occur through overproduction of free radicals and the unregulated production of cellular oxidants
damages DNA, causing mutations and modification of gene expression. These free radicals (e.g. ROS) activate
signal transduction pathways, leading to the transcription of genes
involved in cell growth regulatory pathways, setting the stage for cancer development. This is indicated by, for example, high levels of oxidative lesions in
cancer tissue, and reduced cancer incidence in populations with high
dietary antioxidant intake.
When our protein-controlled
(anti)-oxidant-response doesn’t keep up, oxidative stress causes
oxidative damage that has been implicated in the cause of many diseases
(including cancer) and also has an impact on the body’s aging
Oxidative stress, along with chronic inflammation, has been demonstrated to fuel tumor development cancer cell proliferation, invasion, angiogenesis, and metastasis by activating various oncogenic transcription factors.
It appears that some tumors (adenomas and carcinomas) have increased levels of different markers of oxidative stress, such as increased levels of ROS, nitric oxide (NO), lipid peroxides, and low glutathione levels.
Besides lipid modifications, there is also increased leukocyte activation in carcinogenic tissue, which indicates possible contribution of inflammatory cells to a further oxidative stress and DNA damage.
Consequently, oxidative stress plays a role in the etiology of most cancers, along with the patient’s lifestyle habits (smoking, drinking, use of antioxidants, exercise, etc.). Consistent with that, antioxidant enzymes have been demonstrated to suppress tumorigenesis when being elevated both in vitro and in vivo, making induction of these enzymes a more potent approach for cancer prevention.