Upon activation of oxidative stress, immune cells begin to form free radicals. The synthesis of reactive oxygen species contributes to the development of the inflammatory state. Increased oxidative stress and decreased antioxidant defenses lead to mitochondrial DNA damage and adenosine triphosphate (ATP) depletion. Long-term and constant exposure to free radicals is accompanied by massive damage to molecules. This induces the activation of programmed cell death; in the plasma, the number of mitochondrial fragments increases, which are inducers of the systemic inflammatory response.