Oxidative Stress, Antioxidant and Cancer

Abstract

Oxidative stress is “an imbalance between the systemic manifestation of reactive species and a biological system’s ability to readily detoxify the reactive intermediates or to repair the resulting damage”. Oxidative stress causes by overproduction of reactive species and/or decreased level or dysfunction of antioxidants. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are well recognized for biological effects. Cell damage is a result from interaction between reactive species and cellular biological structure, including lipids and membranes, proteins, sugars, and DNA. Reactive species involve carcinogenesis by direct damage to DNA, growth and proliferation, anti-apoptosis, aggressiveness, and metastasis. Previous studies found higher level of reactive species in cancer patients than control and correlated with poor clinical outcomes. Antioxidants play important role in detoxification of reactive species. Non-enzymatic antioxidants (eg. superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) และ paraoxonase I (PON I)) and enzymatic antioxidants (eg. carotenoids, beta-carotene, lycopene, tocopheral, ascorbate, and glutathione) play role as scavenging and reducing molecule of reactive species. Levels and activities of these antioxidants are usually low, which caused by poor nutritional intake and/or consumption by tumor and normal cells to protect reactive species. In vitro and in vivo data suggested that antioxidants inhibit the growth of tumor cells, however, clinical studies did not prove these benefits, neither carcinogenesis prevention nor efficacy of cancer treatments.