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Although the link between immune system alteration and ASD has long been postulated [38], only in the last decades has the research looked more closely at the potential contribution of the immune system to ASD

Though subsequent events after protein binding were cause for controversy initially (detailed in the section on ferroptosis), progress in resolving this issue was made when it was shown that an oxidant stress was not observed during metabolism of APAP [23, 24] but only after the drug metabolism phase was completed, and that the oxidant stress was located within mitochondria [25, 26]

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