γ-H2AX: A useful tool to detect DNA damage in sudden cardiac death heart tissues, an experimental study

Sudden cardiac death (SCD) is defined as death due to cardiovascular or unidentifiable causes that occurs within an hour of the onset of symptoms. Several lines of evidence suggest that oxidative stress, which is due to an increased production/accumulation of reactive oxygen species (ROS) in cells, may be associated with SCD. ROS can induce DNA damage leading to DNA double-strand break (DSB) that, if not repaired, can lead to cell death. In presence of a DNA DSB, H2AX (a histone H2A variant) is phosphorylated to form γ-H2AX, which binds the DNA DSBs and recruits DNA repair proteins. If DNA damage is excessive and cannot be repaired, cells undergo apoptosis. In the present study, we sought to evaluate the myocardial immunohistochemical expression of γ-H2AX in samples from patients suffering SCD as well as from healthy controls, in order to assess its potential role as a SCD biomarker.