Abstract

Ionizing radiation induces a complex of genetic, biochemical, structural and functional changes in the body. The inflammatory response development is acknowledged as one of the manifestations of systemic bodily response to ionizing radiation exposure, and this response, through the activation of immunity, acts both as protector and leads to the development of undesirable early, delayed and off-target effects. Its underlying molecular and cellular mechanisms are defined by DNA damage, free radical metabolic changes (primarily reactive oxygen and nitrogen species), oxidative stress development, inflammasome activation, “danger signals” release and pro-inflammatory cytokines production. The role of non-apoptotic cell death forms (ferroptosis and pyroptosis) is described in the genesis of post-radiation inflammatory response and subsequent tissue, organ, and system damages. The post-radiation inflammatory reaction’s ability to take form of a time-stable self-sustaining process – that increases the radiation-induced damage severity – due to the presence of a positive feedback between different components of its pathogenesis is noted.

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