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Under oxidative stress, excessive ROS such as OH directly attack DNA, causing single-strand or double-strand breaks, activating PARP-1, consuming NAD and ATP, and generating poly(ADP-ribose), resulting in mitochondrial membrane potential loss and the release of apoptosis-inducing factor, ultimately resulting in cell death [252]
This is due to the fact that in CGD the production of the ROS, hydrogen peroxide, is deficient and so these catalase-positive microorganisms can defeat the limited levels of ROS produced by phagocytic cells
Injectable BPC-157 used in pre-clinical animal research and in off-label clinical settings typically involves higher doses and subcutaneous or intraperitoneal administration
Stubbs G, Litt M, Lis E: Adenosine deaminase activity decreased in autism
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