The idea that even ingestion of the tiniest amount of ragwort will result in damage to an animal's liver is not supported by the science.
First of all neither ragwort itself nor the alkaloids concerned are cumulative in animals. The damage the alkaloids can cause might be if large enough quantities are absorbed and those quantities are enough to overwhelm the inherent natural immunity. The alkaloids would have to be absorbed and there there are a number of factors which will prevent this. These include bacterial destruction inside the digestive tract and then simple failure to be absorbed etc. Then they are not actually not poisonous in themselves until they have been converted into the breakdown produces which are the real toxic substances. We know that these steps of breakdown are not 100% efficient. The mechanisms are covered by Fu et al. in a paper in the journal Drug Metabolism Reviews [1]
The next steps are explained in that paper as follows:-
"Thus, metabolic formation of pyrrolic ester metabolites has been shown to be the primary metabolic activation responsible for the adverse toxicities .............Because of high reactivity, pyrrolic ester metabolites can also react readily with water and other endogenous constituents, such as glutathione, to form the detoxified products."
What this is saying is that there are plenty of things in the cell that detoxify the compounds in ragwort before they have any effect at all.
So damage can only be done at higher doses that over come this resistance.
Glutathione is the substance that makes it possible to consume paracetamol without being poisoned. It is only when the body's supplies of it are depleted that paracetamol becomes toxic. Of course there is plenty of water also to detoxify the compounds in the liver cells.
Then at the next step the toxic breakdown products only exert that toxicity if they come in contact with DNA and there are systems for repairing that damage. It is only after this that the damage can occur and it is only damage that can accumulate not the alkaloids.
It is also notable that the level of immunity to the toxins varies in proportion to the tendency of a given animal species to encounter them. It is evident that this is as a result of evolutionary process creating the right level of immunity as the species co-evolve. Nature shapes animals through natural selection so that they can cope with accidental and normal amounts of poisonous plants that they will encounter naturally. Ragwort poisoning occurs when large quantities are fed in artficial situations in hay or when the animal is starved into eating it.
Another paper makes it clear that there are multiple routes for decomposing the alkaloids in ragwort and not all of them result in toxicity, even though it is rather technical, is one from the American Journal of Veterinary Research [ 2] This points out that there are three ways the compounds can be broken down, only one of which has a toxic effect.
Metabolism of PAs [Pyrrolizidine Alkaloids] occurs by 3 main pathways in the liver. First, to induce toxicosis, PAs can be oxidized by cytochrome P450s to reactive carbonium ion intermediates, which are unstable and either undergo rapid hydrolysis to 6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine (DHP), covalently bind to DNA and other cellular nucleophiles (Figure 1), or both. Thus, DHP is described as the primary toxic metabolite in PA toxicosis.
So this is saying that a group of enzymes (the molecular machines that build or destroy things in living systems) called cytochrome P450s break down the alkaloids into toxic compounds including something with a long name which is called DHP for short.
Second, PAs can be oxidized to N-oxides by P450 and flavin-containing monooxygenase (FMO)enzymes. Pyrrolizidine alkaloid N-oxides are relatively unreactive and are believed to be excreted unchanged in the urine because of their high water solubility.
This says some more enzymes can convert them into other substances which are passed out in urine without doing any harm.
Third, PAs can be hydrolyzed to nontoxic necine base and necic acid moieties via carboxylesterases. Thus, N-oxide formation and hydrolysis are identified as detoxification pathways
And there is another detoxification route with other enzymes.
References
1. Fu PP, Xia QS, Lin G, Chou MW. 2004.Pyrrolizidine alkaloids-Genotoxicity, metabolism enzymes, metabolic activation, and mechanisms.Drug Metab. Rev.36:1-55
2. Duringer, J. M., Buhler, D. R., & Craig, A. M. (2004). Comparison of hepatic in vitro metabolism of the pyrrolizidine alkaloid senecionine in sheep and cattle. American Journal of Veterinary Research, 65(11), 1563-1572.