Dear Colleagues,

Acute ionizing irradiation (IR) affects cell/organ systems with different degrees of injury interfering with life processes. The “primary” radiolytic hit produces direct genotoxic, proteotoxic, and cytotoxic effects, originates oxidative and electrophilic stress and triggers calcium imbalance followed by a wide range of reactive responses driving massive release of the “secondary” paracrine and autocrine stress factors. Eventually, the deleterious targeted and non-targeted IR effects result in either mitosis-linked cell death, or apoptosis or necroptosis—in the dose—limiting tissues; and induce clastogenic and epigenetic responses, up-regulate aseptic inflammation, alter metabolome and induce remodeling—in the systems sustaining adaptation and survival. The residual effects of the “primary” radiolytic impact can persist and propagate in cells/tissues over certain time-period due to exaggerated activation stress-responses or alteration of numerous metabolic mechanisms that includes shift in the cell redox machineries (e.g., endoplasmic reticulum (ER)-mitochondrial network, respiration, constituitive nitric oxide synthase (NOSI), peroxisome, etc.). The deteriorating outcomes of these events are constituted by disbalance of tissue thiols, progressive depletion of redox buffering antioxidants and the protracted oxidative, electrophilic and carbonyl stress. Moreover, the targeted and non-targeted epigenetic response, up-regulation of inflammatory mediators can lead to a long-term expression of pro-oxidant genes (such as inducible nitric oxide synthase, NOSII) sustaining the above. Evidently, the prolonged imbalance of redox mechanisms can contribute to impairment of biological barriers and increase a risk of multiple organ failure. In this light, applications of modulators of: (i) thiol redox balance in tissues and fluids; (ii) mitochondrial redox function; (iii) the ER-stress response and proteostasis; (iv) redox adaptive responses and expression of antioxidant proteins; (v) peroxisome proliferation; (vi) activity of NADPH oxidase 4; and (vii) ROS/RNS-induced cell death, are all under recent consideration for countermeasure against radiation-related effects.

Subjects and aims of the issue:

(i) To address redox biology of radiation injury and targeted redox therapy:

• Interplay between redox metabolome, redox signaling, and aseptic inflammation in sequela of acute radiation disease

• Antioxidants and redox-regulated miRNA in radiation injury

• Antioxidants and phytobiotics in transcriptional and translational regulation of acute radiation response

• Antioxidants and phytobiotics in epigenetic regulation of response

• Mitochondria-targeted antioxidants in mitigation of radiation injury

• Models and techniques for the assessment of the radiation oxidative, electrophilic and carbonyl stress.

(ii) To elucidate the role of antioxidants and other phytobiotics in mechanisms of redox response to ionizing irradiation.

Dr. Nikolai V. Gorbunov
Guest Editor

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• Systems response to ionizing irradiation
• Redox/oxidative stress
• Electrophilic stress
• Redox metabolome
• Reactive carbonyls
• Redox sensors
• Epigenetic regulation of redox signaling
• Inflammation
• Antioxidants
• Phytobiotics