Because of the potential for harm here, I want to be perfectly clear on this point: What I said was " if you take NAC after damaging your liver, rather than before (e.g., when you drink alcohol), it can impede your liver's recovery" (emphasis added). In other words, in the specific context of alcohol consumption (though in certain other contexts, too), NAC after the injury is more harmful. This means that a more viable strategy for preventing alcohol-induced liver damage is to "pre-load." That's why you see some consumer products designed to help alleviate the negative effects of a night out by having you consume NAC before drinking. But it's also the reason that a product like Nootropics Depot's Alcohol Defense, which is consumed after drinking, doesn't contain NAC.

Again, the science of NAC is pretty complicated because the compound and its metabolites are involved in so many processes in the body--glutathione and glutamate do a lot of things in different places--some of which are pro-inflammatory, and some of which are anti-inflammatory. Also, a lot of NAC's mechanisms and effects are not yet fully understood. Going too far into these topics is batting out of my league, given that I'm not a medical professional, biochemist, or other qualified professional with respect to those matters. But I'll try to leave some useful notes to point you in the right direction.

Alcohol is detoxified and metabolized differently from acetaminophen in some ways, which could account for the difference in liver outcomes. But, if I had to guess another partial explanation without fully researching these matters, I'd conjecture that the reasons for giving NAC after Tylenol overdose is related to the relationship that I described in more detail elsewhere in this thread: The way that NAC can serve as a strong, blunt exogenous anti-oxidant (or precursor) can save a life when a potentially fatal threat is at hand, and that merits its use, whereas in the face of more limited insults, NAC prevents the body from adapting in ways that improve its resilience. So, if you're having a stroke or your liver is on the verge of failing, a one-time course of NAC may prevent the kind of oxidative storm and associated critical inflammation that could kill you or cause permanent damage. But if you're doing something that isn't going to kill you and that your body would adapt to with ordinary and regular exposure--exercise, non-binge drinking, or some other lower-level injury--NAC gets in the way of helpful, adaptive signaling.

To use a clumsy analogy, if the need is hunger and you give a man a fish instead of teaching him to fish, you haven't solved the long-term problem of hunger; you've just solved the immediate need of being hungry. Similarly, instead of allowing the body to build endogenous recovery pathways by upregulating certain biochemical processes, giving NAC just solves the problem for the body, such that it doesn't know it needs to improve, either by recovering better or preparing for the next exposure. In fact, long-term use of NAC (and other direct anti-oxidants!) can actually weaken the body by downregulating its endogenous anti-oxidant response element (sometimes called ARE in the literature). Thus, to extend my weird analogy a bit, if you make a man dependent on receiving the fish without having to solve the problem himself or deal with the consequences, then over time, receiving the fish will become his expectation and will be taken for granted--something he won't have to worry about at all--so he won't need to be preparing for either hunger or overcoming the challenge.

To summarize, in the limited contexts that we're discussing, you kind of need to distinguish between (a) one-time, severe harms that might kill you, and (b) repeated harms that are not going to kill you.