3283 Diacetyl Diacetyl is a natural by-product of secondary or malolactic fermentation. It is a vicinal diketone (two C=O groups, side-by-side) with the molecular formula C4H6O2. Carrier of aroma of butter, vinegar, coffee, and other foods. Beer sometimes undergoes a diacetyl rest, which entails waiting two or three days after fermentation is complete, to allow the yeast to absorb the diacetyl it produced earlier in the fermentation cycle. The makers of some wines, such as chardonnay, deliberately promote the production of diacetyl because of the feel and flavors it imparts. 431-03-8 650 C4H6O2 86.036780 Yellow to green liquid (L1280). -2.4°C 88°C 200 mg/mL at 15°C Oral (L1280) ; inhalation (L1280) ; dermal (L1280) ; eye contact (L1280) Diacetyl is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen. Diacetyl is reduced to 2,3-butanediol (A350). LD50: 1580 mg/kg (Oral, Rat) (L1280) LD50: >5 gm/kg (Dermal, Rabbit) (L1280) No indication of carcinogenicity (not listed by IARC). (L135) Carrier of aroma of butter, vinegar, coffee and other foods (A646). Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides. Causes eye irritation, redness and pain. Causes moderate skin irritation. Harmful if swallowed. May cause gastrointestinal irritation with nausea, vomiting and diarrhea. Causes respiratory tract irritation. Vapors may cause dizziness or suffocation. Harmful if inhaled. High exposure to butanedione may cause headache, drowsiness, lack of coordination and seizures (L1280). If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally. 2009-07-30T17:56:41Z 2014-12-24T20:26:01Z http://en.wikipedia.org/wiki/Diacetyl C00741 16583 NN-DIACETYLCHITOBIOSYLDIPHOSPHODOLICHO Diacetyl 1588 true CC(=O)C(C)=O C4H6O2 InChI=1S/C4H6O2/c1-3(5)4(2)6/h1-2H3 InChIKey=QSJXEFYPDANLFS-UHFFFAOYSA-N 86.0892 86.036779436 Endogenous Liquid -1.34 HMDB03407 CHEMBL365809 630 Xu, Ping; Chen, Hong; Du, Yi; Chen, Wanqiu; Xiao, Zijun. Method of preparation diacetyl by oxidization. Faming Zhuanli Shenqing Gongkai Shuomingshu (2005), 6 pp.