Chapter 3 - Oxidative stress and its biological significance

Abstract

Polyunsaturated fatty acids present in the cell membrane are often subject to peroxidation, which leads to various effects in the cell such as reactive oxygen species (ROS) and lipid peroxidation, triggers the path of apoptosis, inhibits cell growth, and finally leads to cell death. Not only higher levels of ROS, but also higher levels of dietary supplementation cause tumorigenesis. ROS produced during normal metabolism in mitochondria attack mtDNA and mitochondrial membrane at the site of production, leading to mitochondrial dysfunction. Oxidative stress is critical in cancer development because ROS can attack genomic DNA (deoxyribonucleic acid) as well as mtDNA, leading to single- or double-stranded damage to DNA, DNA adducts form, DNA bases change results in mutation in DNA leads to various disease. ROS stimulates or inhibits tumorigenesis; it can promote cell growth by mitogenic signaling cascade while suppressing cell growth by genotoxic stress and interrupting protein translation. Foster T cell therapy for tumor cell, in this therapy the ROS level is increased in tumor cells. Smokers are more prone to lung cancer than non-smokers because smoking alters the level of ROS and the inflammatory cytokines level. Tumor cells produce extracellular superoxide anions with the help of NADPH (nicotinamide adenine dinucleotide phosphate) oxidase 1, which protects against the apoptosis of tumor cells. The main objective of a cancer cell is to proliferate and survive; for this, it requires large amounts of energy in a very short time and therefore these cells modify cell metabolism, resulting in low ROS production. Cancer cells prefer energy from glycolysis rather than the electron transport chain.