Why does tylenol impair your liver?
If the liver does not store toxins, why can chronic use of tylenol hurt the liver?
Answers:
because it doesn't have the chance to dispose of them, even if it's not trying to store them because you keep accumulation more and more and more and it can't get rid of it fast enough
The liver does not 'store' toxins.
When you consume tylenol, a very small proportion of it is broken down by CYP450 enzymes into a compound called N-acetyl-p-benzo-quinone imine, or NAPQI. NAPQI is then conjugated to a molecule call glutathione - which the body keeps around to scavenge toxic molecules and remove them through the kidneys.
Since glutathione does not replenish particularly speedily, if you take significant doses of tylenol, you can use the stuff up faster than your body an make it. Each time this happens, the NAPQI specifically not removed damages the liver. Over years, this relatively minor damage can add up.
This is not commonly seen, as the liver tend to start making more glutathione to compensate for its increased usage. It's quite common for vicodin addicts to consume five times the amount of tylenol that would snuff out a normal person and walk away short their liver enzymes so much as spiking.
Tylenol doesn't hurt the liver. But one of its metabolites, n-acetyl-p-benzoquinoneimine (NAPQUI for short) requires glutathione to conjugate with sulfhydryl groups, and if glutathione stores are depleted, the NAPQI is toxic. So long as glutathione stores are adequate, the step goes minus a hitch, and the subsequent end-products are non-toxic. Oddly, there are three pathways for metabolism, and that is in reality not the biggest one.
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Answers:
because it doesn't have the chance to dispose of them, even if it's not trying to store them because you keep accumulation more and more and more and it can't get rid of it fast enough
The liver does not 'store' toxins.
When you consume tylenol, a very small proportion of it is broken down by CYP450 enzymes into a compound called N-acetyl-p-benzo-quinone imine, or NAPQI. NAPQI is then conjugated to a molecule call glutathione - which the body keeps around to scavenge toxic molecules and remove them through the kidneys.
Since glutathione does not replenish particularly speedily, if you take significant doses of tylenol, you can use the stuff up faster than your body an make it. Each time this happens, the NAPQI specifically not removed damages the liver. Over years, this relatively minor damage can add up.
This is not commonly seen, as the liver tend to start making more glutathione to compensate for its increased usage. It's quite common for vicodin addicts to consume five times the amount of tylenol that would snuff out a normal person and walk away short their liver enzymes so much as spiking.
Tylenol doesn't hurt the liver. But one of its metabolites, n-acetyl-p-benzoquinoneimine (NAPQUI for short) requires glutathione to conjugate with sulfhydryl groups, and if glutathione stores are depleted, the NAPQI is toxic. So long as glutathione stores are adequate, the step goes minus a hitch, and the subsequent end-products are non-toxic. Oddly, there are three pathways for metabolism, and that is in reality not the biggest one.
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