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The resulting, locally elevated concentration of pro-inflammatory molecules directly causes hepatocyte injury and apoptosis, for example via TNF-mediated death receptor activation (169), initiating and perpetuating a vicious cycle of necroinflammation leading to loss of hepatocytes and of the livers functional capacity (170)

Thus, understanding the cascade of events initiated by OS is crucial to potentially prevent the amplified cascade of oxidative damage that ultimately leads to the failure of proteins, lipids, and nucleic acids

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