Impact of ROS Generated by Chemical, Physical, and Plasma Techniques on Cancer Attenuation

Abstract

For the last few decades, while significant improvements have been achieved in cancer therapy, this family of diseases is still considered one of the deadliest threats to human health. Thus, there is an urgent need to find novel strategies in order to tackle this vital medical issue. One of the most pivotal causes of cancer initiation is the presence of reactive oxygen species (ROS) inside the body. Interestingly, on the other hand, high doses of ROS possess the capability to damage malignant cells. Moreover, several important intracellular mechanisms occur during the production of ROS. For these reasons, inducing ROS inside the biological system by utilizing external physical or chemical methods is a promising approach to inhibit the growth of cancer cells. Beside conventional technologies, cold atmospheric plasmas are now receiving much attention as an emerging therapeutic tool for cancer treatment due to their unique biophysical behavior, including the ability to generate considerable amounts of ROS. This review summarizes the important mechanisms of ROS generated by chemical, physical, and plasma approaches. We also emphasize the biological effects and cancer inhibition capabilities of ROS.

Keywords: cancers; free radicals; reactive nitrogen species; reactive oxygen species.

Figure 1

Schematic of primary reactive oxygen species (ROS) production mechanism.

Figure 2

Some major intracellular (mitochondria, peroxisome, endoplasmic reticulum (ER) stress, nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidase, metabolizing enzymes) and extracellular (Radiations, Xenobiotics) sources of reactive oxygen species (ROS) generation [81].

Figure 3

Role of reactive oxygen species (ROS) in cancer inhibition by four different mechanisms and the different pathways involved in those mechanisms.

Figure 4

Molecular mechanism of soft-jet plasma-induced cancer cell apoptosis via the mitochondrial intrinsic pathway and extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) activation [250].