Eugenol, C6H3C3H5OCH3OH, is a phenol found in oil of cloves, oil of pimento, and other oils. It is official in the U.S.P. It may be obtained by shaking oil of cloves with excess of a 5 or 10 per cent. solution of sodium hydroxide, drawing off the resulting solution of eugenol-sodium, washing it with ether and decomposing by means of diluted sulphuric acid. The eugenol which separates is washed with solution of sodium bicarbonate and finally distilled with steam or in vacuo. It occurs as a colourless or slightly yellow optically inactive liquid, with an odour of cloves and a pungent spicy taste. Specific gravity, 1.072 to 1.074. Boiling-point, 251° to 253°. It should be entirely and readily soluble in diluted solution of sodium hydroxide. It gives a blue colour on the addition of solution of ferric chloride to its alcoholic solution; on oxidation with potassium permanganate it yields vanillin. Eugenol should be preserved in well-stoppered bottles, protected from the light.
Soluble in all proportions of alcohol, ether, chloroform, or glacial acetic acid.
Action and Uses.—Eugenol is an antiseptic and is not toxic. It has some local anaesthetic properties and is a useful solvent of other local anaesthetics, such as pure cocaine, or erythrophloeine hydrochloride for use in dental practice. It is also used in combination with astringents as a mouth wash after tooth extraction. An antiseptic ointment of eugenol with hydrous wool fat has been used for eczema. Eugenol is administered, in the same manner as oil of cloves in phthisis, as a carminative and antiseptic.
Hepatotoxicity of eugenol in mice depleted of glutathione by treatment with DL-buthionine sulfoximine.
Mizutani T, Satoh K, Nomura H, Nakanishi K.
Department of Food Science and Nutrition, Kyoto Prefectural University, Japan.
Eugenol is widely used as a food flavoring agent and a dental analgesic. Mice treated with eugenol (400-600 mg/kg, po) in combination with an inhibitor of glutathione (GSH) synthesis, buthionine sulfoximine (BSO; 1 hr before eugenol, 4 mmol/kg, ip) developed hepatotoxicity characterized by increases in relative liver weight and serum GPT, hepatic congestion, and centrilobular necrosis of hepatocytes. Eugenol (up to 600 mg/kg) alone produced no hepatotoxicity. Drug metabolism inhibitors such as carbon disulfide, methoxsalen, and piperonyl butoxide prevented or significantly reduced the hepatotoxic effect of eugenol given in combination with BSO. On the other hand, pretreatment with phenobarbital (PB) increased the hepatotoxicity. These results suggest that eugenol is activated by a cytochrome-P-450-dependent metabolic reaction and that the liver injury is caused by inadequate rates of detoxification of the resulting metabolite in mice depleted of hepatic GSH by BSO treatment.
PMID: 2047567 [PubMed - indexed for MEDLINE]
Comparative toxicity of eugenol and its quinone methide metabolite in cultured liver cells using kinetic fluorescence bioassays.
Thompson DC, Barhoumi R, Burghardt RC.
Department of Medical Pharmacology and Toxicology, College of Medicine, Health Science Center, Texas A & M University, College Station 77843, USA.
Comparative kinetic analyses of the mechanisms of toxicity of the alkylphenol eugenol and its putative toxic metabolite (quinone methide, EQM) were carried out in cultured rat liver cells (Clone 9, ATCC) using a variety of vital fluorescence bioassays with a Meridian Ultima laser cytometer. Parameters monitored included intracellular GSH and calcium levels ([Ca2+]i), mitochondrial and plasma membrane potentials (MMP and PMP), intracellular pH, reactive oxygen species (ROS) generation, and gap junction-mediated intercellular communication (GJIC). Cells were exposed to various concentrations of test compounds (1 to 1000 microM) and all parameters monitored directly after addition at 15 s intervals for at least 10 min. Eugenol depleted intracellular GSH, inhibited GJIC and generation of ROS, and had a modest effect on MMP at concentrations of 10 to 100 microM. At high concentrations (1000 microM), eugenol also affected [Ca2+]i, PMP, and pH. Effects of EQM were seen at lower concentrations (1 to 10 microM). The earliest and most potent effects of either eugenol or EQM were seen on GSH levels and GJIC. Coadministration of glutathione ethyl ester enhanced intracellular GSH levels by almost 100% and completely protected cells from cell death caused by eugenol and EQM. These results suggest that eugenol mediates its hepatotoxic effects primarily through depletion of cytoprotective thiols and interference in thiol-dependent processes such as GJIC. Furthermore, our results support the hypothesis that the toxic effects of eugenol are mediated through its quinone methide metabolite.
Just have your IAOMT dentist help you decide.
Everything is toxic when it comes to dental materials.
Once you get your Amalgams out the toxicity from your new fillings will be not worth considering on the scale of things. The amount of nickel, tin, aluminum, barium you ingest and inhale every day will be 100 fold more.
Make sure there is no Marcury, arsenic, chlorine and floride (fluorine) or any deviation of these in the filling. This is just
my opinion... does not mean much.