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However, excessive activation of PARP1 results in the excessive accumulation of poly(ADP-ribose) (PAR) molecules

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Together, this may indicate that chronic oxidative stress caused by the loss of Fh1 exerts its pathophysiological consequence of renal cyst formation in these mice through oxidation of proteins involved in metabolic processes and in maintaining tissue architecture, such as the cytoskeletal and extracellular matrix proteins, despite ROS-scavenging by intracellular, vascular, and urinary proteins

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Vit-C regulates NF-kB release and attenuates pro-inflammatory cytokines production 720