Adapted from Pharmacology by Rang, Dale, Ritter
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Phenacetin and paracetamol in normal therapeutic doses [edit: which may now equate to less than 2g over 48hours] are metabolised into either or both of 2 harmless metabolites; a sulphate or a glucuronide.
However, when doses exceed personal tolerance levels, the cytochrome P450 steps in to "handle the excess" and produces the toxic benzoquinone imine intermediate.
Depending on your levels of the important P450 substrate, glutathione - a natural antioxidant produced in nearly every cell - the toxic imine is converted into a harmless compound which is excreted.
When Glutathione is depleted, the imine reacts with cell proteins which results in the death of the cell.
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Glutathione must be synthesised within the cell. Levels are thought to vary somewhat between individuals, and are not easily increased. Giving the amino acid cystine, one of the 3 starting amino acids, is not thought to raise levels by much and presents other health concerns, and glutathione administered intravenously has a very short half life.
It’s possible the combination of E and paracetamol could potentiate the effects of glutathione depletion. I’m not saying it definitely would, but as MDMA also uses P450 cytochromes when available, care should be exercised, as it should with any new drug type, dosage or combination.