Alkaloids
Ciguatera poisoning
Grayanotoxin (honey intoxication)
Hormones from the thyroid glands of slaughtered animals (especially Triiodothyronine in cases of hamburger thyrotoxicosis or alimentary thyrotoxicosis)
Mushroom toxins
Phytohaemagglutinin (red kidney bean poisoning; destroyed by boiling)
Pyrrolizidine alkaloids
Shellfish toxin, including paralytic shellfish poisoning, diarrhetic shellfish poisoning, neurotoxic shellfish poisoning, amnesic shellfish poisoning and ciguatera fish poisoning
Scombrotoxin
Tetrodotoxin (fugu fish poisoning)Some plants contain substances which are toxic in large doses, but have therapeutic properties in appropriate dosages. Foxglove contains cardiac glycosides. Poisonous hemlock (conium) has medicinal uses. Other pathogenic agents
Prions, resulting in Creutzfeldt–Jakob disease (CJD) and its variant (vCJD)

"Ptomaine poisoning"
Ptomaine poisoning was a myth that persisted in the public consciousness, in newspaper headlines, and legal cases as an official diagnosis, decades after it had been disproven scientifically in the 1910s.In the 19th century, the Italian chemist Francesco Selmi, of Bologna, introduced the generic name ptomaine (from Greek ptōma,  "fall, fallen body, corpse") for alkaloids found in decaying animal and vegetable matter, especially (as reflected in their names) putrescine and cadaverine. The 1892 Mercks Bulletin stated, "We name such products of bacterial origin ptomaines; and the special alkaloid produced by the comma bacillus is variously named Cadaverine, Putrescine, etc." While The Lancet stated, "The chemical ferments produced in the system, the... ptomaines which may exercise so disastrous an influence." It is now known that the "disastrous... influence" is due to the direct action of bacteria and only slightly due to the alkaloids. Thus, the use of the phrase "ptomaine poisoning" is now obsolete.
Interactions
Drug–drug interactions
Naproxen may interact with antidepressants, lithium, methotrexate, probenecid, warfarin and other blood thinners, heart or blood pressure medications, including diuretics, or steroid medicines such as prednisone.NSAIDs such as naproxen may interfere with and reduce the efficacy of SSRI antidepressants, as well as increase the risk of bleeding greater than the individual bleeding risk of either class of agent, when taken together. Naproxen is not contraindicated in the presence of SSRIs, though concomitant use of the medications should be done with caution. Alcohol consumption increases the risk of gastrointestinal bleeding when combined with NSAIDs like naproxen in a dose-dependent manner (that is, the higher the dose of naproxen, the higher the risk of bleeding). The risk is highest for people who are heavy drinkers. Pharmacology
Mechanism of action
Naproxen works by reversibly inhibiting both the COX-1 and COX-2 enzymes as a non-selective coxib. Pharmacokinetics
Naproxen is a minor substrate of CYP1A2 and CYP2C9. It is extensively metabolized in the liver to 6-O-desmethylnaproxen, and both the parent drug and the desmethyl metabolite undergo further metabolism to their respective acylglucuronide conjugated metabolites. An analysis of two clinical trials shows that naproxens time to peak plasma concentration occurs between 2–4 hours after oral administration, though naproxen sodium reaches peak plasma concentrations within 1–2 hours. Pharmacogenetics
The pharmacogenetics of naproxen has been studied in an effort to better understand its adverse effects.