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Tylenol NAPQI Cancer

Type: Image (jpeg)

Submitter: [anonymous]

Category: Political

Exhibition Date: 2018-08-20 12:23:04 MST

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Submitter's Comment
Paracetamol's (aka Tylenol, Acetaminophen, Nyquil, Dayquil and Various other brands for pain, cold, flu, fever) active metabolites i
are AM404 (a cannabinoid) and NAPQI (a powerful toxin).

Pharmaceutical corporations such as Bayer, Tylenol and other companies which convert Phenol, Benzene and other petrochemicals into synthetic drugs, fibers, pesticides and preservatives, have spent billions annually on laws for the repression of natural drugs and herbs which would offer safe and effective alternatives to OTC and percription drugs.

Paracetamol use by the mother during pregnancy is associated with an increased risk of childhood asthma.[97] It is also associated with an increase in ADHD but it is unclear whether the relationship is causal.[98] A 2015 review states that paracetamol remains a first-line recommended medication for pain and fever during pregnancy, despite these concerns.[99]

Studies have found an association between paracetamol and a increase in kidney, liver and bladder cancer risks.[101]

Mechanism of action

AM404 – Metabolite of paracetamol

Anandamide – Endogenous cannabinoid
The mechanism of action of paracetamol is not completely understood. Unlike NSAIDs such as aspirin, paracetamol does not appear to inhibit the function of any cyclooxygenase (COX) enzyme outside the central nervous system, and this appears to be the reason why it is not useful as an anti-inflammatory.[102] It does appear to selectively inhibit COX activities in the brain, which may contribute to its ability to treat fever and pain.[102] This activity does not appear to be direct inhibition by blocking an active site, but rather by reducing COX, which must be oxidized in order to function.[102]

It also appears that paracetamol might modulate the endogenous cannabinoid system in the brain through paracetamol's metabolite, AM404. AM404 appears to inhibit the reuptake of the endogenous cannabinoid/vanilloid anandamide by neurons, making it more available to reduce pain. AM404 also appears to be able to directly activate the TRPV1 (older name: vanilloid receptor), which also inhibits pain signals in the brain.[102]


Main pathways of paracetamol metabolism (click to enlarge). Pathways shown in blue and purple lead to non-toxic metabolites; the pathway in red leads to toxic NAPQI.
After being taken by mouth it is rapidly absorbed by the gastrointestinal (GI) tract (although absorption through the stomach is negligible);[103] its volume of distribution is roughly 50 L.[104] The concentration in serum after a typical dose of paracetamol usually peaks below 30 µg/ml (200 µmol/L).[105] After four hours the concentration is usually less than 10 µg/mL (66 µmol/L).[105]

Paracetamol is metabolised primarily in the liver, into toxic and non-toxic products. Three metabolic pathways are notable:[86]

Glucuronidation (45-55%),[3] by UGT1A1 and UGT1A6;[101]
Sulfation (sulfate conjugation) (20–30%)[3] by SULT1A1;[101]
N-hydroxylation and dehydration, then glutathione conjugation, (less than 15%). The hepatic cytochrome P450 enzyme system metabolises paracetamol (mainly CYP2E1), forming a minor yet significant alkylating metabolite known as NAPQI (N-acetyl-p-benzoquinone imine) (also known as N-acetylimidoquinone).[86][106] NAPQI is then irreversibly conjugated with the sulfhydryl groups of glutathione.[106]
All three pathways yield final products that are inactive and eventually excreted by the kidneys. In the third pathway, however, the intermediate product NAPQI is toxic. NAPQI is primarily responsible for the toxic effects of paracetamol; this constitutes an example of toxication.[107] Production of NAPQI is due primarily to two isoenzymes of cytochrome P450: CYP2E1[101] and CYP3A4

Keywords: NAPQI, corruption, drug war, kidney cancer, liver damage, opium wars, poppy tea, hemp, CBD, CBC, FDA

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