DO NOT UNDER ANY CIRCUMSTANCES EVER, EVER !!!!!!EVER!!!!!!! permit a dog access to grapes, raisins or other grape products!!!
GRAPES ARE LETHAL TO MOST DOGS (a small minority are apparently unaffected but most are not)
It does not take much, even a small child-sized serving may well prove fatal to even a big adult dog!!!
Its well known about chocolate being dangerous to dogs, but grapes can be much more dangerous and in less quantity too.
Worse yet, are if one gets hold of any product containing the sweetener xylitol (one of the sugar alcohols, don't know if other polyol 'sugar alcohols' such as pentaerythritol fr.ex are also toxic, but it wouldn't come as any surprise). This one is worse yet, even a tiny quantity can be rapidly fatal to a dog, the amount contained in just a couple of those tiny sugar free 'smint' mint sweets is enough to kill a large dog. Same with sugar free chewing gum sweetened with xylitol, although the outcome is more likely to be treatable if responded to before the onset of symptoms and the dog rushed to a vet and the situation explained.
Canines cannot metabolize xylitol, and it causes a sustained, massive release of insulin, and corresponding prolonged and intensely severe, profound hypoglycaemic shock, if this ever does happen to a dog, sugar, ideally glucose but table sugar, (bring the fucking bags of it and use as necessary) dissolved in water when needed to be used needs to be brought with you along with a bottle to give it, or if you have to a feeding syringe, to liquefy into a concentrated solution and stick it up the dog's arse if they become comatose (which can happen rapidly in cases of xylitol poisoning for rapid absorption and of course the dog being unable to swallow if comatose due to the insulin-shock) whilst transporting to the vet, where they will be put on a glucose drip line.
In the case of grapes and grape products the cause is less known, it may be due to a mycotoxin (fungus-produced toxin). The result is rapid-onset kidney failure which may easily progress to fulminant, fatal presentation of total kidney failure.
Also, the sulfur compounds in onions, garlic and similar Alliaceous plants are toxic to dogs. Xylitol toxicity in dogs is to be considered extreme. It is also of very, very rapid onset (ten minutes to a half hour for an average sized dog. Probably on the lower end of the scale for a small dog and the higher end for a very large dog, of course dose dependent-the larger the dose the greater the rapidity, assuming the same individual dog under the same conditions, with which a given proportion of a given quantity can enter the system of the dog in question, same of course goes for any other living entity (at least, animals, not sure about plants, thats probably down more to the means of delivery and and to what surface area and where, as for single-celled organisms, there concentration gradients are going to play a part as well as strain, since uptake is either active (what it sounds like) or passive via diffusion, diffusion rate constant is probably, I'd guess much the same for a species with a given composition of cell wall whilst transport-mediated uptake is going to be much more variable, due to things like transporter occupation at any given time for a given substrate, ability of the competing (I.e toxin being uptaken) ligand to displace the bound ligand from transporters already occupied, affinity of the pre-bound ligand for the target transporter or antiporter), the existence of antiporters (similar to a transporter, only functioning in the opposite direction, and intracellular, serving to pump out a substrate or substrates from the cell the antiporter is located within to the extracellular environment from the cytoplasm, some of dedicated function and some, such as in humans, the p-glycoprotein found in the blood-brain barrier walls, as multidrug efflux-pumps, removing for examples amongst synthetic substrates, quinidine [a cardiac drug for arrythmias], the antidiarrheal drug loperamide [immodium, and if it got into the brain, both an extremely long acting, and highly potent opioid. Some people have abused it, or used it in desparation as a means to attempt to taper without getting fucked by the pork, in megadose levels, and often, combined with a p-glycoprotein inhibitor, sometimes not, though and relying solely on the transporter being saturable, and at a certain, although large level, 100mg at least, probably more, its been enough to floor heroin addicts and have them come round in hospital, only to pass out again after the very short acting naloxone used as an emergency antidote for opiate overdoses wears off and they fall back under the influence of the loperamide, after taking sufficient that some crosses the BBB and acts centrally. Unfortunately there are also two major downsides other than the obvious, I.e never, ever, ever shitting again, either in this life, the next, or anybody elses be the somebody else mortal or otherwise
and those being one-it gets metabolized, as does haloperidol, into a nasty charged quaternary ammonium derivative, once it enters cells via monoamine oxidase-B, from whence it can thus, due to the permanent charge, no longer leave, in this case the metabolite is known as LPP+ an N-methylphenylpyridinium species, structurally related to the notorious poison MPTP and the charged metabolite of it that does the damage, MPTP, which, akin to the loperamide metabolite, which normally never gets to do any damage, because it never gets into the brain, or rather, it does, just barely, because it can cross the BBB, but it is a substrate for p-glycoprotein which immediately grabs it and spits it out under normal conditions [normal being when the efflux pump is not saturated by massive doses of loperamide, blocked by compounds that inhibit p-glycoprotein or compete with loperamide for uptake capacity thus lowering the loperamide dose required to cause central effects] and any molecule of loperamide situated nearby that just made a break for it, and tries again just gets given the snatch-and-chucked-out-the-window treatment by the 'bouncer' of the 'nightclub' in question. And repeat as necessary until its metabolized peripherally. The other problem, aside from metabolism into a parkinsonian neurotoxin is that it also has a propensity in massive quantities such as are used in that manner, for causing cardiac arrythmia, as it prolongs the Q-T wave interval of the heart's electrical rhythm. IIRC via inhibition of hERG (human ether-a-go-go related gene, getting its rather hilarious name from the action the activation of its protein transcript in Drosophila, the genus of fruit-flies commonly used as lab model organisms in testing things, in part due to their rapid lifecycle, easy diet (rotting fruit), and when mutated, which is if distasteful, extremely practical due to the rapidity of a new generation being formed, and growing, if the mutation be nonlethal, to maturity, as well as often dramatic, and just as much hideous and vile as dramatic, owing to things like say, legs growing out of where their antennae should be, eyeballs in the wrong places, no eyeballs, or worse things besides, the name of the hERG protein and its coding gene, arising from the acute effects of ether on the living flies, if I remember right, at least in people, the ion channel it encodes, is a potassium channel, and whilst I cannot remember the rectification direction, its a well-known antitarget tested for in drug development, since its excessive activation can induce cardiac arrhythmia.)
In the case of xylitol, anyhow, the dose required is very small. It may take as little as a single piece of sugar-free chewing gum to poison a dog. It can be in toothpaste, sweets, chewing gum, diabetic foods and others, if you have a dog, do not have products containing xylitol in the house, or if you do, keep them, and their refuse, chewed gum included, locked away and where it cannot be accessed. A large dog may take longer to show symptoms for a given dose whilst a smaller one will very likely show a much more rapid onset. Onset can be as fast as 10 minutes in any case to as long as a half hour. Massive insulin release with consequent profound hypoglycaemic shock; and also liver failure, in very severe cases. Prompt response on even suspecting ingestion of xylitol-containing foodstuffs or other xylitol-containing products essential or the result is one or more fucked dogs. And I don't mean the type that happens when bored single women get kinky, given a sizable paycheck or both.
http://www.petmd.com/dog/emergency/digestive/e_dg_grape_raisin_toxicity Grapes seem to target the kidneys. Most but not all dogs susceptible. Quantity of grape or raisins etc. required to cause toxicity and rapid-onset kidney failure:quite small, although larger than the miniscule amount of the extremely toxic (for dogs) xylitol. Not that that is saying much.
http://www.petmd.com/dog/conditions/endocrine/c_dg_xylitol_toxicity?page=showParacetamol is also toxic to dogs. And IIRC highly toxic to cats. Especially to autisti..I mean...cats. Oops. my bad there, easy mistake to make, loveable, often cute and snuggly, about the same inborn propensity towards herd formation or joining as flatworms have for developing advanced spaceflight technology, trainable-if they feel like it. Will do some things trained for, again if they feel like it. Always come when called and extremely sociab.......oh...wait. Confirmation-two wrongs do not, indeed, make a right.
