Blonde Roof Rat

Why We Put These Three Things In The Water

By · 31 min read · Updated

Start here, because it changes how you should read the rest

Three things go into our rats’ drinking water: ergothioneine, betaine, and taurine. This page is the argument for why, written the way I would want to read it if someone else were making the case to me.

Before any of it, the honest footing. A PubMed title-and-abstract search on 2026-09-06 for roof rats (Rattus rattus, roof rat, black rat, ship rat) together with each compound returned nothing: no records for ergothioneine, none for betaine, none for taurine. The same species terms return 52 records when paired with the kidney instead, so the search works and the shelf really is empty. Everything below comes from work done in Norway rats, in mice, in cats, in pigs and cattle and poultry, in human cells, and in people. Roof rats and Norway rats are different animals, which is the whole reason this site exists, and I am not going to quietly borrow one and call it the other.

So read this as a reasoned bet, not a result. The chemistry and the physiology are solid and are shared across mammals. The step from “this is how the mammalian kidney handles betaine” to “this is good for my roof rats” is an inference, and it is mine. Where the inference is strong I will say so. Where it is thin I will say that too, and there are places below where it is thin.

One more piece of framing, in the order we actually hold it: ergothioneine is the important one. Taurine and betaine are the supporting cast. That ordering is not a hedge. It falls out of the argument in the next section, and it is worth keeping in mind if you ever have to pick just one.

The problem this mix is answering

Our rats eat a formulated block as the base of the diet, and that is the right call. A good extruded block is the easiest way to feed a rat a complete, safe, balanced diet, and we say so on our ultra-processed pet food page. This is not an anti-kibble argument.

But making that block is a trade. The dough is milled, cooked at roughly 110 to 150 C under pressure for a matter of seconds, puffed, and dried.[1] That process buys real things: gelatinized starch a rat can actually digest, destroyed trypsin inhibitors and lectins that would otherwise damage the gut,[2] a genuine pathogen kill step,[3] shelf stability, and the enormous practical virtue that every piece is identical so a rat cannot pick out the fatty bits and leave the balanced part behind.

What it costs is a set of fragile things. Heat-labile vitamins take real losses, with vitamin A and thiamine the best documented.[4][5][6] The Maillard browning that makes the food smell good also locks up some lysine in a form the body cannot use.[7] Plant polyphenols are reduced and altered.[8] Fragile fats oxidize.

Here is the hinge of the whole thing, and it is the sentence to hold onto:

The manufacturer tops back up the nutrients that are on the spec sheet. Nothing tops up the ones that were never on it.

Makers know extrusion destroys heat-labile vitamins, so they deliberately overdose the vitamin premix and coat the fragile ones on after drying.[4] The block comes out nutritionally complete against its label, and that is a real achievement. But “complete” means complete against a list of required nutrients written decades ago.[9] It does not mean complete against everything a wild-foraging omnivore’s body is built to expect.

That gap, the things nobody is measuring because nobody put them on the list, is what this mix is aimed at. It is not a multivitamin. A multivitamin would be redundant with the premix. It is three specific compounds chosen because each one is missing or thin for a different, nameable reason, and because between them they cover three cellular systems that do not overlap.[10][11][12]

The three, one at a time

Ergothioneine: the one a milled block has no source for

This is the strongest case in the mix by a wide margin, and it rests on a fact about where the molecule comes from.

No animal can make ergothioneine. Not rats, not us, not anything with a backbone. It is produced by certain fungi and soil bacteria, and every molecule of it in an animal’s body arrived by mouth.[10] A food’s ergothioneine content is essentially a readout of the living soil and fungal world that food grew in.[13]

Now look at a lab block. Milled grains and oilseeds, cooked, dried, sterile. There is no mushroom in it and no soil-microbe layer in it, because both were the point of removing them. So the reasonable expectation is that a captive rat on a block diet gets very little ergothioneine, and possibly close to none.[10][13]

I want to be precise about the strength of that claim, because it is the load-bearing one. I searched for such a measurement and did not find one, and our own ultra-processed page already flags this same point as an inference rather than a lab result. What is measured is where the compound is made and that animals cannot make it.[10] The step to “therefore kibble has none” is logic, not chemistry on a plate. It is good logic. It is still logic.

What makes the gap worth caring about rather than shrugging at is how the body treats the stuff. There is a single dedicated doorway for it, a transporter called OCTN1, and it is the only way in: knock the transporter out in a mouse and tissue ergothioneine is essentially gone.[14] Rats have a working version of that same transporter, which is a large part of why rodent work on ergothioneine transfers at all.[15] Once absorbed, it is held onto rather than excreted, with very little urinary loss.[16] Bodies do not build a dedicated private door and then hoard what comes through it for something they do not need.

The pointed part, for anyone keeping rats: ergothioneine concentrates in the kidney,[17] and age-related kidney disease is common in rats. Chronic progressive nephropathy, a spontaneous age-related kidney disease, occurs at high incidence in the rat strains used in toxicology, increasing with age and hitting males harder.[18] Those are Norway rats in laboratories rather than pet roof rats, so read it as the closest measured population and not as a mortality figure for your own animals. In rat models it protects that tissue,[19][20] and there is a nasty loop where chronic kidney disease itself lowers blood ergothioneine by wrecking the intestinal transporter that absorbs it.[17] The organ that most wants the compound is the organ whose failure cuts off the supply.

And the animal results are not small. Low daily ergothioneine, given in the drinking water from young and continued for life, raised median lifespan in male mice.[21] In aged animals it improved endurance and muscle through a genuinely novel route: it is not a raw material for NAD+ the way NMN and NR are, it is a trigger, feeding an enzyme that releases a small hydrogen-sulfide signal that switches the NAD+ machinery back on.[22] In people, it has been argued as a “longevity vitamin” that modern diets under-supply.[23]

So: a compound animals cannot synthesize, that a processed diet has no plausible source of, that the body guards like something essential, that concentrates in the organ pet rats most often lose, and that extended lifespan in mice. That is why it is first.

Taurine: the amino acid that plants do not carry

Rats make their own taurine. That is true, and it is the honest starting point, because it means this is not a deficiency correction the way taurine in cat food was. Cats cannot make enough, their food stopped supplying it, and they went blind and died of heart failure until the industry reformulated.[24] Rats are not in that position. Anyone who tells you otherwise is selling something.

So why add it at all? Two reasons, and I will give the weaker one first.

The weaker reason is the supply side. Taurine is an animal-tissue compound. Plants contain essentially none, so the soy, corn and wheat that make up most of a rodent block contribute none.[25] A block with fish meal in it carries some; a purely plant-protein one carries almost nothing.[11] And because rats synthesize their own, nobody fortifies to a target, so no one can tell you how much is in the bag. The result is that a rat on a plant-protein block is running on endogenous synthesis alone, with essentially no preformed dietary contribution on top. That is adequate. It is not necessarily generous, and tissue taurine content does shift with age in rats.[26]

The stronger reason is what taurine does that nothing else in the mix does.[27] It is physically built into the mitochondrial protein factory. A subset of mitochondrial transfer RNAs carry a taurine-derived modification at the wobble position, and that modification is required for those tRNAs to read their codons correctly when mitochondria build their own proteins.[27] Lose it and mitochondrial translation falters.[27] Taurine deficiency produces a strikingly similar pattern, because without enough taurine the modification cannot be made.[28] This is not antioxidant hand-waving. Taurine is a component part of the machine.[27][28]

Layered on that: it sits at roughly 20 millimolar in cardiac muscle, about a hundred times its plasma level, supporting calcium handling and contractility.[29] It protects the rat kidney against oxidative injury and reduces calcium-oxalate crystal deposition, which is the most directly relevant piece of evidence any of the three compounds has for a rat-keeping concern.[30] It reacts with neutrophil-derived hypochlorous acid to form taurine chloramine, which damps inflammatory signalling, and in a colony carrying endemic Mycoplasma that means limiting the chronic inflammatory damage rather than fighting the organism.[31] And in stressed or aging male rats it improved sperm count, motility and testosterone.[32][33]

Where the taurine case is weakest, said plainly: the reproductive gains were mostly in stressed or aged animals rather than healthy young ones, and a study that looked for an effect on litter size found none.[34] The aging headline, that taurine declines with age and restoring it extends healthspan, is real work but it is recent and partly contested.[35] And taurine gets the largest spoon of the three, which makes it look like the centrepiece. It is not. It gets the largest spoon because it is the compound the body holds at millimolar concentrations in tissue, so a meaningful top-up is simply a larger quantity of material. Size of spoon is not rank of importance.

Betaine: the methyl budget nobody thinks about

Betaine is the one most easily dismissed, and it is in the mix for a structural reason rather than a glamorous one.

Every cell constantly moves single-carbon methyl groups onto DNA, RNA, proteins and phospholipids.[36] Those reactions set gene expression, build membranes and clear metabolites. The currency is S-adenosylmethionine, and keeping it supplied means recycling homocysteine back into methionine. There are two routes for that step. One runs on folate and B12. The other runs on betaine directly, through an enzyme called betaine-homocysteine methyltransferase, which is most active in liver and kidney.[37] Ergothioneine cannot do this. Taurine cannot do this. It is a system the other two never touch.

Three things follow. Methylation capacity gets supported, and methylation capacity declines measurably with age.[38] Homocysteine gets cleared, which is well enough established that betaine anhydrous is an approved human prescription treatment for homocystinuria.[39] And folate gets spared, because when betaine handles the recycling the folate pathway is relieved of it and that folate stays available for DNA and RNA synthesis. The sparing runs both ways: deprive an animal of choline and betaine and it burns more folate to recycle homocysteine, and deprive it of folate and it leans harder on choline and betaine.[36] The reason to care about that most during growth, recovery and lactation is reasoning rather than a measured result: those are the times when methylation and DNA synthesis draw hardest on the same pool.

Betaine is also a kidney-medulla osmolyte, taken up by its own transporter, BGT-1, and used by medullary cells to hold their shape and protect their proteins against the brutal salt gradient the kidney makes to concentrate urine.[40] Note where that is. Ergothioneine concentrates in the proximal tubule.[17] Betaine works in the medulla. Same organ, different rooms.

And the honest weakness, which is real: betaine is already in the food. It occurs naturally in cereal grains, and wheat bran and wheat germ are among the richest sources there are, at roughly 1,300 mg per 100 g each,[12] so a grain-based block already supplies some. It is even used deliberately as a feed additive for its methyl-sparing effect.[41] So unlike ergothioneine, this is not filling a hole that processing opened. It is topping up something that is present in an unknown and unlabelled amount, against a target for roof rats that nobody has ever established. That is a weaker argument and it should be read as one. The reason it is still worth doing is that the dose is small, the compound is cheap, the downside at nutritional intake is not evident, and the system it supports is the one system the other two leave entirely uncovered.

Why three, and why not one

The case for the combination is not that they stack. It is that they do not overlap.[10][12][27]

Sort them by mechanism and they land in three different places. Ergothioneine is a redox and signalling molecule that works through a private transporter and a hydrogen-sulfide-to-NAD+ cascade.[10][22] Taurine is a structural component of mitochondrial translation, an osmolyte, a bile-acid conjugator and an anti-inflammatory agent.[27][31] Betaine is a methyl donor and a medullary osmolyte.[37][40] There is no shared pathway where a third one is doing what the first two already did.

Sort them by tissue and the same thing happens inside a single organ. In the kidney alone, ergothioneine concentrates in the proximal tubule,[17] betaine defends the medulla,[40] and taurine acts as a broad antioxidant and anti-crystal agent across the nephron.[30] Three compounds, three compartments, one organ that is a leading cause of death in old pet rats.

Sort them by what processing did and you get the ordering again. Ergothioneine: the block has no plausible source, so this is the clearest case of the three. Taurine: the block has essentially none preformed if it is plant-protein-based,[11] but the rat makes its own, so this is a top-up rather than a hole. Betaine: the block has some, amount unknown, so this is insurance.[12]

That is the honest hierarchy, and it is why the ergothioneine page is the long one and this is the order we keep. Drop to one compound and you should keep ergothioneine.[10] Drop to two and add taurine.[11][12] Betaine is the third leg of the stool: not the largest, but the one that keeps the other two from leaving a whole branch of cellular maintenance unsupported.[12]

One boundary worth naming, so nobody reads this as a complete answer to what processing removes. These three are in the water because they dissolve and dose cleanly. Fats do not, which is why omega-3, another real casualty of a processed diet,[42] is handled separately and is a problem we have not fully solved here. The water trinity is three of the gaps, not all of them.

The dose, and why the spoon is the specification

The dose is: one eighth teaspoon of ergothioneine, one eighth teaspoon of betaine, and one half teaspoon of taurine, per US gallon of drinking water.

That is the specification. It is not a rounding of some underlying milligram target. The teaspoon is the thing that actually happens in this house, and every concentration below is arithmetic done off it rather than the other way round.

That is not laziness, and this is the part I want to spend a paragraph on, because it is genuinely interesting and it changed how our own dosing calculator is written.

A powder does not have one weight per spoonful. Bulk density, how much mass fits in a given volume, depends on the shape of the crystal, and for taurine the crystal shape is itself the property manufacturers engineer.[43] A fine needle-shaped taurine packs at about 0.51 g per mL.[43] Blocky, non-agglomerating crystals grown deliberately for flowability come in at 0.64 to 0.73.[43] Recrystallized taurine reaches 0.90 to 1.10.[44] A supplement-grade product specification gives 0.7 to 0.9 g per mL loose.[45]

Run half a teaspoon of each of those into a gallon and the answer ranges from about 330 to about 720 mg per litre. That is more than a twofold spread, and every one of those numbers is a real published figure for real taurine. There is no single true milligram number for half a teaspoon. There never was. Which is exactly why the spoon is the specification and the concentration is the derived, approximate quantity, and why our dosing calculator now leads with the spoon.

Narrowing to the supplement-grade band, the sort of jar someone keeping rats would actually buy, half a teaspoon lands at roughly 460 to 590 mg per litre.[45] The calculator uses 520, from inside that band.

The other two are tighter but built the same way. Betaine anhydrous at 97 percent has a published bulk density of 0.50 to 0.70 g per mL,[41] so an eighth of a teaspoon is roughly 80 to 115 mg per litre, and the calculator uses 100. An ergothioneine powder certificate of analysis lists 0.65 g per mL,[46] which puts an eighth of a teaspoon at about 105 mg per litre. One caveat on that last one, because it is my inference and not the document’s word: that certificate labels its row only “Density”, not “bulk density”, and I am reading it as a bulk figure.

And a rule for reading any number on this page: if a milligram figure ever disagrees with the spoon, the spoon wins. The spoon is what gets measured out.

What we cannot tell you, and will not make up

You will notice there is no “milligrams per rat per day” figure in this section. That is deliberate.

To get from milligrams per litre to milligrams per rat you need to know how much water a rat drinks in a day, and the intake figure behind our numbers is a looked-up one rather than a measurement of these animals. Averages are averages: a rat who drinks more than average takes in proportionally more, and a young growing rat drinks more for her size than an adult does.

So the per-animal number is knowable, and it is knowable by weighing a bottle. No measurement of drinking from this colony has been published here. Until there is one, treating a per-rat figure as a fact would be dressing up an assumption as a measurement. We would rather leave the hole visible.

Why the dose is balanced

Three separate senses of balanced, because the word is doing three jobs.

Balanced against what the compounds are for. The proportions are not arbitrary and they are not equal. Taurine gets four times the spoon of the other two because it is the one the body carries at millimolar concentrations in tissue,[29] so a meaningful contribution is simply more material. Ergothioneine gets an eighth of a teaspoon because it works at low concentrations through a saturable transporter and because the rodent benefits appeared at low daily doses, not high ones.[21] Betaine gets an eighth of a teaspoon deliberately: it is included at a nutritional level, comparable to what a betaine-rich diet would provide, not a pharmacological one.

Balanced against each other’s failure modes. This one is not obvious and it matters. Betaine is a methyl donor, and a pharmacological betaine dose has a documented cost: 6 grams a day for six weeks raised LDL cholesterol and triglycerides in healthy people, enough to work against the homocysteine benefit it was given for.[47] Keeping betaine at a nutritional level, rather than scaling it up to match taurine, is what keeps the mix from becoming a methylation intervention.[47] Similarly, taurine is a growth substrate as well as a protectant,[48] which is a real consideration covered below, and a maintenance quantity keeps that in proportion.

Balanced against the diet it sits on top of. None of these three are being used to fix a formulation error. The block is doing the heavy lifting for protein, fat, vitamins and minerals, and this mix is not competing with it. Betaine is arguably the clearest example: it is already in a grain-based block,[12] so the water is topping up rather than supplying.

Why it is safe, and the exact limits of that

Ergothioneine has the widest margin of the three, and it is not close. The no-adverse-effect level in rats is 800 mg per kg of body weight per day, established with no genotoxicity and no reproductive toxicity.[49] A separate one-generation rat reproduction study found no effect on fertility and no maternal or developmental toxicity.[50] Set that against the doses at which benefit actually appeared: the mouse lifespan work used a low daily dose in drinking water,[21] and the aged-animal healthspan work likewise operated well below any toxic range.[22] The useful doses and the harmful ones are separated by orders of magnitude, and ergothioneine is approved as a novel food in the EU.[49]

Taurine’s margin can be stated without any assumption about drinking, which is the cleanest kind of safety comparison available here. The maternal study that flagged caution at high taurine used 1.5 percent in the drinking water,[34] which is 15,000 mg per litre. Our concentration is in the region of 500. That is a factor of roughly thirty, comparing one water concentration to another, with no water-intake figure needed in the middle. Meanwhile the published rat supplementation work that produced benefits used doses that sit above our figure rather than below,[33] which is worth saying plainly: this is a modest daily top-up, not a therapeutic dose.

Betaine’s safety case rests on it being small on purpose. Betaine anhydrous is an approved human prescription drug for homocystinuria,[39] which tells you the compound is well characterized in people at therapeutic doses. Ours is a nutritional quantity, in the same region as what a betaine-rich food supplies: wheat bran and wheat germ run around 1,300 mg per 100 g.[12] The documented downsides sit at much larger doses. Six grams a day for six weeks raised LDL cholesterol and triglycerides in healthy people,[47] and a diet of 1 percent betaine through pregnancy and lactation raised liver and blood cholesterol in the offspring of the rats fed it.[51] A nutritional dose stays well below the amounts where those effects were seen, and that is the reason betaine is not scaled up.

The three caveats we will not bury

Taurine and existing cancers. Some cancers, notably myeloid leukemia, import taurine through the same transporter healthy tissue uses, and use it as metabolic fuel.[48] In a healthy colony at maintenance quantities this is theoretical. In an individual animal with an existing blood cancer it is not theoretical, and additional taurine could in principle feed the thing you want starved. Taurine is a building block, and building blocks get used by whatever is growing.[48] If a rat has a diagnosed tumour, this is a conversation to have with a vet rather than a decision to make from a web page.

Betaine, for what it is worth, points the other way in the cancer literature we have: it suppressed rather than supported cancer stem-cell properties in liver cancer models, through the same methylation pathway.[52] Ergothioneine is genuinely two-sided and honestly split: tumours can build extra OCTN1 doorways, but ergothioneine has also been shown to kill colorectal cancer cells outright.[53] Nobody should claim this is settled in either direction.

More is not better, for any of the three. Ergothioneine’s benefit runs through a hydrogen-sulfide signal,[22] and a signal that helps as a pulse is not a thing you want as a flood. That is the ordinary U-shaped dose-response nearly every nutrient has, from folate to selenium to iron to water itself. What is unusual about ergothioneine is how wide the safe window is,[49] not that it lacks one.

The species gap is the real limit on all of this. Every safety number above was established in Rattus norvegicus or in another species entirely. Roof rats share the relevant transporters and enzymes as far as anyone knows, because these are deeply conserved systems, but “as far as anyone knows” is carrying weight in that sentence. This is the one caveat that no amount of margin fixes, and it applies to the benefit claims exactly as much as to the safety ones.

Is it effective? How strong that word can honestly be

Here is where I have to be careful, because this is the question a reader most wants a confident answer to and the one where confidence would be least earned.

What is demonstrated, in some animal, by somebody: ergothioneine extends median lifespan in male mice[21] and improves endurance and muscle in aged animals;[22] it protects the rodent kidney against injury;[19] taurine reduces oxidative injury and crystal deposition in the rat kidney[30] and its mitochondrial tRNA role is established biochemistry;[27] betaine’s methyl-donor pathway and its medullary osmolyte role are established physiology.[37][40] These are not in dispute.

What is inference: that a formulated block leaves a real ergothioneine gap. Strong inference, since no animal makes the compound and the block has no fungal or soil-microbe source, but nobody has put a rodent block in a mass spectrometer and published the number.

What is untested: that giving these three compounds, at these quantities, in the water, to roof rats, produces a measurable benefit. Nobody has run that study. We have not run it either. Our colony has been on this mix for months, and what that gives us is an absence of anything going visibly wrong, which is worth something as a tolerability signal and worth nothing at all as evidence of benefit. There is no control group. There is no blinding. There is no endpoint anyone is measuring. A colony that looks well is a colony that looks well.

So the honest summary is this. This is a defensible bet, not a demonstrated result. The bet is that three cheap, well-tolerated, mechanistically distinct compounds, aimed at gaps a processed diet plausibly leaves, with wide safety margins in the closest species anyone has studied, are more likely to help than to hurt over a rat’s short life. I think that bet is a good one and I have taken it with my own animals. I am not going to tell you it has been proven, because it has not, and the day someone shows me it does not work I would rather have written this page honestly than have to walk back a claim I made too loudly.

What would change the picture, in the order I would want it done: measure ergothioneine in commercial rodent blocks, so the load-bearing inference becomes a measurement. Weigh water bottles, so per-animal intake stops being a looked-up average. And if anyone with a real colony and a real control group wants to run the actual experiment, we will publish the result whichever way it lands. Our open research questions page is where things like this live.

The short version

Processing takes out fragile things and puts back only the ones on the spec sheet. Ergothioneine was never on any spec sheet, no animal can make it,[10] and a sterile milled block has nowhere to get it from, which makes it the strongest case in the mix and the one to keep if you keep only one. Taurine is a top-up rather than a hole, since rats make their own, but plant-protein blocks supply essentially none preformed[25] and taurine is physically built into the mitochondrial protein factory.[27] Betaine is insurance on a system the other two never touch, at a deliberately nutritional dose.[12][47]

The dose is the spoon: an eighth, an eighth, and a half, per gallon. Milligram figures are derived from that and are approximate, because powders genuinely do not have one weight per spoonful.[43]

Safety margins are wide, the widest by far for ergothioneine, and the taurine comparison holds up without any assumption about how much a rat drinks. The caveats we will not bury are existing cancers and taurine, the ordinary fact that more is not better, and the species gap that underlies everything here.

And every word of it is extrapolated from animals that are not roof rats. That is not a disclaimer at the bottom. It is the shape of the whole argument.

This is educational information about nutrition, not veterinary advice. No supplement replaces a vet. A rat with laboured breathing, weight loss, or any sudden change needs veterinary care.

Further reading

References

  • [1] Tran QD, Hendriks WH, van der Poel AFB. “Effects of extrusion processing on nutrients in dry pet food.” Journal of the Science of Food and Agriculture 2008;88(9):1487-1493. DOI.
  • [2] Pasqualone A, Costantini M, Coldea TE, Summo C. “Use of legumes in extrusion cooking: a review.” Foods 2020;9(7):958. PubMed.
  • [3] Anderson NM, Keller SE, Mishra N, et al. “Salmonella Inactivation During Extrusion of an Oat Flour Model Food.” Journal of Food Science 2017;82:738-743. PubMed.
  • [4] Morin P, Gorman A, Lambrakis L. “A literature review on vitamin retention during the extrusion of dry pet food.” Animal Feed Science and Technology 2021;277:114975. DOI.
  • [5] Galli GM et al. “Stability of vitamin A at critical points in pet-feed manufacturing and during premix storage.” Frontiers in Veterinary Science 2024;11:1309754. PubMed.
  • [6] DiSabatino B, et al. “In extruded feline diets, thiamine degraded at a similar rate when stored at -20°C, compared to room temperature.” Canadian Veterinary Journal 2021;62(4):374-378. PubMed.
  • [7] van Rooijen C, Bosch G, van der Poel AFB, Wierenga PA, Alexander L, Hendriks WH. “The Maillard reaction and pet food processing: effects on nutritive value and pet health.” Nutrition Research Reviews 2013;26(2):130-148. DOI.
  • [8] Šárka E et al. “Changes in phenolics during cooking extrusion: a review.” Foods 2021;10(9):2100. PubMed.
  • [9] National Research Council (US) Subcommittee on Laboratory Animal Nutrition. “Nutrient Requirements of Laboratory Animals: Fourth Revised Edition, 1995.” National Academies Press 1995. source.
  • [10] Borodina I, Kenny LC, McCarthy CM, et al. “The biology of ergothioneine, an antioxidant nutraceutical.” Nutrition Research Reviews 2020;33(2):190-217. PubMed.
  • [11] Li P, Wu G. “Composition of amino acids and related nitrogenous nutrients in feedstuffs for animal diets.” Amino Acids 2020;52(4):523-542. PubMed.
  • [12] Zeisel SH, Mar MH, Howe JC, Holden JM. “Concentrations of choline-containing compounds and betaine in common foods.” Journal of Nutrition 2003;133(5):1302-1307. PubMed.
  • [13] Carrara JE, Lehotay SJ, Lightfield AR, Sun D. “Linking soil health to human health: Arbuscular mycorrhizae play a key role in plant uptake of the antioxidant ergothioneine from soils.” Plants, People, Planet 2023. DOI.
  • [14] Kato Y, Kubo Y, Iwata D, et al. “Gene knockout and metabolome analysis of carnitine/organic cation transporter OCTN1.” Pharmaceutical Research 2010;27(5):832-840. PubMed.
  • [15] Nakamura T et al. “Functional characterization of ergothioneine transport by rat organic cation/carnitine transporter Octn1 (slc22a4).” Biological & Pharmaceutical Bulletin 2008;31(8):1580-1584. PubMed.
  • [16] Cheah IK, Tang RMY, Yew TSZ, Lim KHC, Halliwell B. “Administration of Pure Ergothioneine to Healthy Human Subjects: Uptake, Metabolism, and Effects on Biomarkers of Oxidative Damage and Inflammation.” Antioxidants & Redox Signaling 2017;26(5):193-206. PubMed.
  • [17] Shinozaki Y, Furuichi K, et al. “Impairment of the carnitine/organic cation transporter 1-ergothioneine axis is mediated by intestinal transporter dysfunction in chronic kidney disease.” Kidney International 2017;92(6). PubMed.
  • [18] Hard GC, Khan KN. “A contemporary overview of chronic progressive nephropathy in the laboratory rat, and its significance for human risk assessment.” Toxicologic Pathology 2004;32(2):171-180. PubMed.
  • [19] Salama SA, Abd-Allah GM, Mohamadin AM. “Ergothioneine mitigates cisplatin-evoked nephrotoxicity via targeting Nrf2, NF-kB, and apoptotic signaling and inhibiting gamma-glutamyl transpeptidase.” Life Sciences 2021;278:119572. PubMed.
  • [20] Dare A, Channa ML, Nadar A. “L-ergothioneine and its combination with metformin attenuates renal dysfunction in type-2 diabetic rat model by activating Nrf2 antioxidant pathway.” Biomedicine & Pharmacotherapy 2021;141:111921. PubMed.
  • [21] Katsube M et al. “Ergothioneine promotes longevity and healthy aging in male mice.” GeroScience 2024;46:3889-3909. PubMed.
  • [22] Petrovic D et al. “Ergothioneine improves healthspan of aged animals by enhancing cGPDH activity through CSE-dependent persulfidation.” Cell Metabolism 2025;37(2):542-556.e14. PubMed.
  • [23] Beelman RB et al. “Is ergothioneine a longevity vitamin limited in the American diet?.” Journal of Nutritional Science 2020;9:e52. PubMed.
  • [24] Pion PD et al. “Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy.” Science 1987;237:764-768. PubMed.
  • [25] Rana SK, Sanders TA. “Taurine concentrations in the diet, plasma, urine and breast milk of vegans compared with omnivores.” British Journal of Nutrition 1986;56(1):17-27. PubMed.
  • [26] Eppler B, Dawson R Jr. “Cysteine sulfinate decarboxylase and cysteine dioxygenase activities do not correlate with strain-specific changes in hepatic and cerebellar taurine content in aged rats.” Mechanisms of Ageing and Development 1999;110(1-2):57-72. PubMed.
  • [27] Kirino Y, Yasukawa T, Ohta S, et al. “Codon-specific translational defect caused by a wobble modification deficiency in mutant tRNA from a human mitochondrial disease.” Proceedings of the National Academy of Sciences USA 2004;101(42):15070-15075. PubMed.
  • [28] Schaffer SW, Jong CJ, Warner D, Ito T, Azuma J. “Taurine deficiency and MELAS are closely related syndromes.” Advances in Experimental Medicine and Biology 2013;776:153-165. PubMed.
  • [29] Huxtable RJ. “Physiological actions of taurine.” Physiological Reviews 1992;72(1):101-163. PubMed.
  • [30] Li CY, Deng YL, Sun BH. “Taurine protected kidney from oxidative injury through mitochondrial-linked pathway in a rat model of nephrolithiasis.” Urological Research 2009;37(4):211-220. PubMed.
  • [31] Park E, Schuller-Levis G, Quinn MR. “Taurine chloramine inhibits production of nitric oxide and TNF-alpha in activated RAW 264.7 cells by mechanisms that involve transcriptional and translational events.” Journal of Immunology 1995;154(9):4778-4784. PubMed.
  • [32] Yang J, Wu G, Feng Y, et al. “Effects of taurine on male reproduction in rats of different ages.” Journal of biomedical science 2010;17 Suppl 1(Suppl 1):S9. PubMed.
  • [33] Adedara IA, Alake SE, Adeyemo MO, et al. “Taurine enhances spermatogenic function and antioxidant defense mechanisms in testes and epididymis of L-NAME-induced hypertensive rats.” Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2018;97:181-189. PubMed.
  • [34] Kabasakal Çetin A, Alkan Tuğ T, Güleç A, et al. “Effects of maternal taurine supplementation on maternal dietary intake, plasma metabolites and fetal growth and development in cafeteria diet fed rats.” PeerJ 2021;9:e11547. PubMed.
  • [35] Singh P, Gollapalli K, Mangiola S, et al. “Taurine deficiency as a driver of aging.” Science 2023;380(6649):eabn9257. PubMed.
  • [36] Niculescu MD, Zeisel SH. “Diet, methyl donors and DNA methylation: interactions between dietary folate, methionine and choline.” Journal of Nutrition 2002;132(8 Suppl):2333S-2335S. PubMed.
  • [37] Parkhitko AA et al. “Methionine metabolism and methyltransferases in the regulation of aging and lifespan extension across species.” Aging Cell 2019;18(6):e13034. PubMed.
  • [38] Zawieja E et al. “Betaine and aging: A narrative review of findings, possible mechanisms, research perspectives, and practical recommendations.” Ageing Res Rev 2025;104:102634. PubMed.
  • [39] U.S. Food and Drug Administration. “CYSTADANE (betaine anhydrous) for oral solution: prescribing information.” DailyMed, U.S. National Library of Medicine. link.
  • [40] Kempson SA, Montrose MH. “Osmotic regulation of renal betaine transport: transcription and beyond.” Pflugers Archiv – European Journal of Physiology 2004;449(3):227-234. PubMed.
  • [41] EFSA Panel on Additives and Products or Substances used in Animal Feed (FEEDAP). “Safety and efficacy of betaine anhydrous for food-producing animal species based on a dossier submitted by AB Vista.” EFSA Journal 2018;16(7):e05335. PubMed.
  • [42] Lin S, Hsieh F, Huff HE. “Effects of lipids and processing conditions on lipid oxidation of extruded dry pet food during storage.” Animal Feed Science and Technology 1998;71(3-4):283-294. DOI.
  • [43] Wanhua Chemical Group Co Ltd. “CN109574886A: Taurine crystal with improved bulk density and flowability that does not agglomerate, and its preparation method.” China National Intellectual Property Administration (via Google Patents) 2019. link.
  • [44] Zhejiang NHU Co Ltd. “CN112479944A: Taurine and its recrystallization method.” China National Intellectual Property Administration (via Google Patents) 2021. link.
  • [45] Xi’an Healthful Biotechnology. “Taurine Powder product specification.” link.
  • [46] ProVita Biotech. “Bulk L-Ergothioneine Powder, certificate of analysis.” link.
  • [47] Olthof MR, van Vliet T, Verhoef P, Zock PL, Katan MB. “Effect of homocysteine-lowering nutrients on blood lipids: results from four randomised, placebo-controlled studies in healthy humans.” PLoS Medicine 2005;2(5):e135. PubMed.
  • [48] Sharma S, Rodems BJ, Baker CD, et al. “Taurine from tumour niche drives glycolysis to promote leukaemogenesis.” Nature 2025;644(8075):263-272. PubMed.
  • [49] EFSA NDA Panel. “Safety of synthetic l-ergothioneine (Ergoneine) as a novel food pursuant to Regulation (EC) No 258/97.” EFSA Journal 2016;14(11):4629. DOI.
  • [50] Forster R, Spézia F, Papineau D, et al. “Reproductive safety evaluation of L-Ergothioneine.” Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 2015;80:85-91. PubMed.
  • [51] Zhao N, Yang S, Feng Y, Sun B, Zhao R. “Enhanced hepatic cholesterol accumulation induced by maternal betaine exposure is associated with hypermethylation of CYP7A1 gene promoter.” Endocrine 2019;64(3):544-551. PubMed.
  • [52] Wang C, Li MC, Huang WG, et al. “Betaine inhibits the stem cell-like properties of hepatocellular carcinoma by activating autophagy via SAM/m6A/YTHDF1-mediated enhancement on ATG3 stability.” Theranostics 2025;15(5):1949-1965. PubMed.
  • [53] D’Onofrio N, Martino E, Balestrieri A, et al. “Diet-derived ergothioneine induces necroptosis in colorectal cancer cells by activating the SIRT3/MLKL pathway.” FEBS Letters 2022;596(10):1313-1329. PubMed.
Explore more topics
The Line & DomesticationNews about this siteHealth & MedicalHusbandry & CareBehavior & SocialWild vs Domestic