OXIDATIVE STRESS BASED-BIOMARKERS IN ORAL CARCINOGENESIS: A REVIEW

Abstract

Human cancer development is a multistep process. A variety of endogenous and exogenous stimuli trigger a complex series of cellular and molecular changes that contribute to cancer formation, one of which is the creation of reactive oxygen species (ROS). Oral cancer is one of the most deadly health issues that humanity faces today. Oral cancer accounts for 2% to 3% of all cancers and is the 5th most frequent disease worldwide, according to the World Health Organization (WHO). Oxygen derived species such as hydrogen peroxide, superoxide anion radical, hydroxyl radical (OH•), and singlet oxygen are well known to be cytotoxic and have been implicated in the etiology of a wide array of human diseases, including oral cancer. Various carcinogens may also partly exert their effect by generating reactive oxygen species (ROS) during their metabolism. Mutations can result from oxidative damage to cellular DNA, which could have a role in the onset and advancement of multistage carcinogenesis (including mouth cancer) via a variety of processes. ROS has an impact on central cellular processes such proliferation, apoptosis, and senescence, all of which have been linked to cancer development. Antioxidant deficiency or an oxidant-antioxidant imbalance can cause oxidative damage to cellular macromolecules, which can lead to cancer. Understanding the significance of reactive oxygen species (ROS) as essential mediators in signaling pathways may open up new avenues for pharmaceutical intervention. We review the current state of knowledge on the role of these oxidative modified cellular byproducts in serving as reliable biomarkers for oral cancer detection, prognosis and diagnosis.