Panado and Paracetamol : Cat killers
According to a new study, paracetamol toxicity for cats may be due to an important hepatic enzymatic deficiency in this species. Paracetamol, a potentially dangerous drug for cats Paracetamol is an analgesic drug often used in human medicine. Most of the time, it is self-administer in order to relieve little pains without the need of practitioners’ advice.
Moreover for people, this drug seems to be really easy to use and truly efficient; therefore it appears as a reflex to give paracetamol to their pets when they undergo fever or pain. Cats are very sensitive to paracetamol: 250 mg could kill a cat.
However, what is good for us is not necessarily good for them. If most owners know that chocolate can kill a dog they often ignore that paracetamol can poison their cats. For these reasons, veterinarians regularly treat cats suffering from fever, mouth-watering, shivering, and comas: symptoms of paracetamol poisoning.
Paracetamol is specifically toxic for cat liver. Cat liver is an essential organ to filter blood and avoid cat intoxication by xenobiotics (foreign molecules in the organism). Indeed, liver drains an important part of the arterial flow and all the intestinal tract flow too. Liver cells are very rich in hepatic enzymes which permit transformations in order to store or degrade xenobiotics.
Toxicity is not a question of molecule but a question of dose, so paracetamol could be toxic for any species. However, paracetamol toxic dose are 3 to 5 times lower in cats compared with humans or dogs. According to Michael H. Court and David J. Greenblatt, from Tufts University, Boston School of Medicine “Cat half-life paracetamol is prolonged”.
This means that paracetamol is not normally eliminated by the cat metabolism. Furthermore, they noticed a significant formation of a ‘highly reactive oxidative component’ (paracetamol derivated molecule which could damage cells
An enzymatic deficiency is responsible for the poor paracetamol degradation. In order to study this heightened sensitivity at paracetamol, Michael H. Court and David J. Greenblatt’s team tried to model cat paracetamol metabolism. That is why they compared paracetamol degradation rapidity by hepatic enzymes in seven different species including cats. At the same time, they assessed the degradation capacity of two types of laboratory rats: a witness group and another group with a hepatic enzymatic genetical deficiency.
This study first highlighted that enzyme maximum degradation rapidity is 10-fold lower for cats than for other animals. This characteristic of the cat hepatic enzyme may be one of the major reasons of the cat exacerbated sensitivity to paracetamol. Rat models gave the scientists a second reason explaining this sensitivity.
Indeed rats with a deficient expression of hepatic enzyme responsible of the paracetamol degradation had the same reaction as cats in the presence of paracetamol. Thus, this rat models showed that cat paracetamol sensitivity may also be due to a lower level of expression of the cat hepatic enzyme.
Human drugs are not directly transposable to veterinary medecine. This new study explains at last an aspect of the cat paracetamol intoxication biological origin. This article will permit the veterinarians to explain more clearly to their clients why they can’t give paracetamol to their cats. Moreover, Aspirin and other anti-inflammatory drugs also have an important toxicity for cats. So it appears very important to educate the pet owners: they should not give human drugs to their pets without asking advice to their veterinarian.
Biochemical Pharmacology, Vol. 53, pp. 1041-1047, 1997 Molecular basis for deficient acetaminophen glucuronidation in cats, Michael H. Court and David J. Greenblatt