Short Overview of ROS as Cell Function Regulators and Their Implications in Therapy Concepts

Abstract

The importance of reactive oxygen species (ROS) has been gradually acknowledged over the last four decades. Initially perceived as unwanted products of detrimental oxidative stress, they have been upgraded since, and now ROS are also known to be essential for the regulation of physiological cellular functions through redox signaling. In the majority of cases, metabolic demands, along with other stimuli, are vital for ROS formation and their actions. In this review, we focus on the role of ROS in regulating cell functioning and communication among themselves. The relevance of ROS in therapy concepts is also addressed here.

Keywords: cancer; cellular processes; metabolism; physiology; reactive oxygen species (ROS); redox signaling; therapy.

Figure 1

Generation of reactive oxygen species (ROS) and their impact on cells. This is a simplified scheme representing exogenous (e.g., UV light, ionizing radiation, pharmaceuticals, etc.) and endogenous sources (e.g., electron transport chain in mitochondria, NADPH (nicotinamide adenine dinucleotide phosphate) oxidases, peroxisomes, endoplasmic reticulum, etc.) of ROS formation. Cells have evolved antioxidative mechanisms (e.g., glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), etc.) that fine-tune ROS levels, ensuring normal cellular functioning. Thus, depending on the levels, ROS affect different transcription factors, enzymes, and/or other proteins, inducing signaling pathways that assure proper functioning and, in general, health. In contrast, higher levels of ROS lead to irreversible damage of macromolecules, thus eventually leading to disease. Again, depending on the levels, ROS impact cellular functions such as proliferation, differentiation, and apoptosis.

Figure 2

Procarcinogenic and anticarcinogenic roles of ROS.

Figure 3

Interconnected cancer-growth-supportive alterations and factors.