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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)

J Neurochem 86:228237 Gegg ME, Clark JB, Heales SJR (2005) Co-culture of neurones with glutathione deficient astrocytes leads to increased neuronal susceptibility to nitric oxide and increased glutamate-cysteine ligase activity

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