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Summarizing the available data from animal studies, we can conclude that oxidative damage of the brain during treatment with typical antipsychotics is due to the following mechanisms: A significant decrease in the activity of Mn-SOD, Cu,Zn-SOD, and catalase Increased lipid peroxidation of membranes Reduction of NO concentration [345] Increased production of superoxide and H 2 O 2 [345] Human studies also indicate that antipsychotics contribute to oxidative stress [346]

The Complexity of Oxidative Stress in Human Age-Related Diseases-A Review

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Some recent studies on metabolic support highlight the benefits of B12 in this process

The most important of these is blood sample collection (taking blood samples from subjects within a time frame after the drug has been administered) and the interval for blood collection should be determined by the drug's properties

Ammonia potentiates GABAA response in dissociated rat cortical neurons