Talk:NAPQI

message: I've added a new reference with a lot of additional detail about the mechanism of NAPQI toxicity.  It seems that the mechanism diagram, in addition to the faults that Dr. Gresely identified five years ago (!), is also misleading.  Specifically, it gives the distinct impression that toxicity results from unconjugated NAPQI, when in fact the NIH reference makes clear that depletion of glutathione itself is also very likely a contributor to the toxic effects of NAPQI.  The potential mechanisms for toxicity from the NIH article are of course too detailed and too uncertain for inclusion in the article proper, but nevertheless make for fascinating reading. Ataru (talk) 08:49, 18 February 2013 (UTC)
thread_title:  Update 

message: The clarification for the use of paracetamol versus acetaminophen seems unnecessary in an otherwise short article. I don't believe the naming needs to be justified either way in the main article. All of the clarification that is really needed is in the first sentence cf. "paracetamol (acetaminophen)." Maybe the defense of appropriate terminology can be taken care of outside of the article.  — Preceding unsigned comment added by 67.239.224.51 (talk) 23:14, 16 August 2012 (UTC)
thread_title:  General Information 

message: NAPQI in the mechanism diagram has he wrong structure. It should be a quinone not a phenol. The structure of the glutathioine conjugate product is also wrong. The reaction is a conjugate addition involving the removal of a double bond, not its addition. 
87.127.28.229 (talk) 10:06, 30 December 2007 (UTC)
thread_title:  Mechanism for Metabolism 

message: The article states that acetylcysteine can be given without risk of side effects.
This is inaccurate and is even contradicted in the main article for Acetylcysteine 82.47.1.14 (talk) 16:21, 24 March 2008 (UTC)
replies: text:  The actual mechanism of NAQPI toxicitiy seems to be its covalent binding to and subsequent inactivation of several critical cell proteins by arylation, inducing a cell death cascade. This occurs rapidly after ingestion, within several hours. The NAQPI-induced oxidation of enzymes alters the cell's normal functioning and impairs its defense against reactive oxygen species, giving way to even more extensive oxidation and cell damage. It was commonly thought that this was an irreversible process, but current toxicology research seems to point to a process that can be prevented, interrupted, and even reversed after the inital covalent binding. (Currently, I'm not at work (this is 'work' for me), but I'll try and get some more info on the subject, including references.) Mfhulskemper (talk) 14:20, 24 April 2009 (UTC)
thread_title:  Acetylcysteine Side Effects 

message: As I recall it, the increase in NAQPI formation was *thought* to be due to saturation of the glucuronidation pathway, BUT current standards point to saturation of *sulfation rates* as the main culprit. Glucuronidation is now thought to be saturated ONLY in individuals with a severe paracetamol intoxication. (Of course, cytochrome P450 metabolism varies greatly and therefore the NAQPI formation may differ from patient to patient as well.) Mfhulskemper (talk) 14:20, 24 April 2009 (UTC)
thread_title:  Sulfation vs. glucuronidation 

message: Why is the suicide information part of the toxicology? This should not be included under the toxicology heading.  —Preceding unsigned comment added by 71.80.125.28 (talk) 01:18, 18 April 2011 (UTC)
thread_title:  Toxicology and Suicide? 

message: The 3D model shows one of the double bonds of the benzoquinone ring in the wrong position, as a consequence you can see that there is a carbon atom with only three bonds, the Carbon-Nitrogen bond is also wrongly shown as a single bond when it should be a double bond.  — Preceding unsigned comment added by 37.237.84.32 (talk) 14:54, 19 January 2022 (UTC)
replies: text: I agree, so I have removed the image.  Reba16 (talk) 00:19, 19 July 2022 (UTC)
thread_title:  Wrong double bond position and a missing double bond