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Hepatic effects that are considered adverse include death, abnormal clinical chemistry parameters, obvious functional organ impairment, DNA and mitochondrial alteration, glutathione depletion, hepatocyte necrosis, enhanced replicative DNA synthesis, generation of reactive oxygen species, and increased peroxisome proliferation (in rodents) (Williams and Iatropoulos 2002)

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Further analysis suggested the role of transforming growth factor--dependent, preferential induction of T-regulatory cells in this immune adaptation