Reactive oxygen species (ROS), either endogenously generated or derived from the environment, are usually removed by the physiological antioxidant mechanisms of the cell; whenever ROS production exceeds the scavenging capability of the biological system, cells undergo oxidative stress, and their molecular component—proteins, lipids, nucleic acids—may be seriously damaged.

The cellular effects of oxidative stress depend on the response of the different organelles and the extent of the induced damages. In the presence of severe injury, cell death may occur by catastrophic events (i.e., by necrosis) or by regulated forms (such as apoptosis, parthanatos, and anoikis). Conversely, in the presence of a mild oxidative stress, the cells may activate metabolic responses which promote repair and survival.

A variety of physical or chemical stimuli may be used under controlled conditions to induce oxidative stress, in the attempt to either selectively cause cell damage and death or to activate cell metabolism. The scope of this special issue is to elucidate the potential of oxidative stress as a powerful versatile tool for multiple biomedical applications. Scientists working on a wide variety of topics, such as development, aging, cancer, cardiovascular, and neuromuscular and neurodegenerative diseases in cellular and animal model systems as well as in humans are encouraged to submit a paper.

Potential topics include, but are not limited to:

• Apoptosis
• Anoikis
• Necrosis
• Parthanatos
• Autophagy
• Organelle damage and repair
• Cell nuclear activities