The acetyl moiety is a component of many organic compounds, including acetic acid, the neurotransmitter acetylcholine, acetyl-CoA, acetylcysteine, acetaminophen (also known as paracetamol), and acetylsalicylic acid (also known as aspirin).
The introduction of an acetyl group into a molecule is called acetylation. In biological organisms, acetyl groups are commonly transferred from acetyl-CoA to other organic molecules. Acetyl-CoA is an intermediate both in the biological synthetase and in the breakdown of many organic molecules. Acetyl-CoA is also created during the second stage of cellular respiration, pyruvate decarboxylation, by the action of pyruvate dehydrogenase on pyruvic acid.
Histones and other proteins are often modified by acetylation. For example, on the DNA level, histone acetylation by acetyltransferases (HATs) causes an expansion of chromatin architecture, allowing for genetic transcription to occur. However, removal of the acetyl group by histone deacetylases (HDACs) condenses DNA structure, thereby preventing transcription.
Acetylation can be achieved using a variety of methods, the most common one being via the use of acetic anhydride or acetyl chloride, often in the presence of a tertiary or aromatic amine base. A typical acetylation is the conversion of glycine to N-acetylglycine:
There is some evidence that acetyl-L-carnitine may be more effective for some applications than L-carnitine. Acetylation of resveratrol holds promise as one of the first anti-radiation medicines for human populations.
The term was coined by Justus von Liebig in 1839 to denote what he believed to be the radical of the acetic acid, and what we now call the vinyl group (coined in 1851). When it became a scientific consensus that his theory was wrong and the acid had a different radical, the name was carried over to the correct one, but the name of acetylene (coined in 1860) was retained.
The changes in the muscle contents of CoASH and carnitine and their acetylated forms, lactate and the active form of pyruvate dehydrogenase complex were studied during incremental dynamic exercise. Eight subjects exercised for 3-4 minutes on a bicycle ergometer at work loads corresponding to 30, 60 and 90% of their VO2max. Muscle samples were obtained by percutaneous needle biopsy technique at rest, at the end of each work period and after 10 minutes of recovery. During the incremental exercise test there was a continuous increase in muscle lactate, from a basal value of 4.5 mmol kg-1 dry weight to 83 mmol kg-1 at the end of the final period. The active form of pyruvate dehydrogenase complex increased from 0.37 mmol acetyl-CoA formed per minute per kilogram wet weight at rest to 0.80 at 30% VO2max, 1.28 and 1.25 at 60 and 90% VO2max, respectively. Both acetyl-CoA and acetylcarnitine increased at the two highest work loads. The increase of acetyl-CoA was from 12.5 mumol kg-1 dry weight at rest to 27.3 after the highest work load and for acetylcarnitine from 6.0 mmol kg-1 dry weight to 15.2. The CoASH and free carnitine contents fell correspondingly. There was a close relationship between acetyl-CoA and acetylcarnitine accumulation in muscle during exercise, with a binding of approximately 500 mol acetyl groups to carnitine for each mole of acetyl-CoA accumulated. The results imply that the carnitine store in muscle functions as a buffer for excess formation of acetyl groups from pyruvate catalyzed by the pyruvate dehydrogenase complex.
This study investigated intramuscular triacylglycerol (IMTG) and glycogen utilisation, pyruvate dehydrogenase activation (PDHa) and acetyl group accumulation during prolonged moderate intensity exercise. Seven endurance-trained men cycled for 240 min at 57 % maximal oxygen consumption (V(O2,max)) and duplicate muscle samples were obtained at rest and at 10, 120 and 240 min of exercise. We hypothesised that IMTG utilisation would be augmented during 2-4 h of exercise, while PDHa would be decreased secondary to reduced glycogen metabolism. IMTG was measured on both muscle samples at each time point and the coefficient of variation was 12.3 +/- 9.4 %. Whole body respiratory exchange ratio (RER) decreased from 0.89 +/- 0.01 at 30 min to 0.83 +/- 0.01 at 150 min and remained low throughout exercise. Plasma glycerol and free fatty acids (FFAs) had increased compared with rest at 90 min and progressively increased until exercise cessation. Although plasma glucose tended to decrease with exercise, this was not significant. IMTG was reduced at 120 min compared with rest (0 min, 15.6 +/- 0.8 mmol kg(-1) d.m.; 120 min, 12.8 +/- 0.7 mmol kg(-1) d.m.) but no further reduction in IMTG was observed at 240 min. Muscle glycogen was 468 +/- 49 mmol kg(-1) d.m. at rest and decreased at 120 min and again at 240 min (217 +/- 48 and 144 + 47 mmol kg(-1) d.m.). PDHa increased above rest at 10 and 120 min, but decreased at 240 min, which coincided with reduced whole body carbohydrate oxidation. Muscle pyruvate and ATP were unchanged with exercise. Acetyl CoA increased at 10 min and remained elevated throughout exercise. Acetylcarnitine increased at exercise onset but returned to resting values by 240 min. Contrary to our first hypothesis, significant utilisation of IMTG occurred during the first 2 h of moderate exercise but not during hours 2-4. The reduced utilisation of intramuscular fuels during the last 120 min was offset by greater FFA delivery and oxidation. Consistent with the second hypothesis, PDHa decreased late in moderate exercise and closely matched the estimates of lower carbohydrate flux. Although the factor underlying the PDHa decrease was not apparent, reduced pyruvate provision secondary to diminished glycolytic flux is the most likely mechanism.
In organic chemistry, acetyl (ethanoyl), is a functional group, the acyl of acetic acid, with chemical formula -COCH3. It is sometimes abbreviated as Ac (not to be confused with the element actinium). The acetyl radical contains a methyl group single-bonded to a carbonyl. The carbon of the carbonyl has a lone electron available, with which it forms a chemical bond to the remainder R of the molecule.
The acetyl radical is a component of many organic compounds, including the neurotransmitter acetylcholine, and acetyl-CoA, and the analgesics acetaminophen and acetylsalicylic acid (better known as aspirin).
The introduction of an acetyl group into a molecule is called acetylation (or ethanoylation). In biological organisms, acetyl groups are commonly transferred bound to Coenzyme A (CoA), in the form of acetyl-CoA. Acetyl-CoA is an important intermediate both in the biological synthesis and in the breakdown of many organic molecules.
Acetyl groups are also frequently added to histones and other proteins modifying their properties. For example, on the DNA level, Histone acetylation by acetyltransferases (HATs) causes an expansion of chromatin architecture allowing for genetic transcription to take place. Conversely, removal of the acetyl group by histone deacetylases (HDACs) condenses DNA structure, thereby preventing transcription.
When acetyl groups are bound to certain other organic molecules, they impart an increased ability to cross the blood-brain barrier. This makes the drug reach the brain more quickly, making the drug's effects more intense and increasing the effectiveness of a given dose. Acetyl groups are used to make the natural antiinflammitant salicylic acid into the more effective acetylsalicylic acid, or aspirin. Similarly, they make the natural painkiller morphine into diacetylmorphine, or heroin.
N-acetylaspartate (NAA) is a highly abundant brain metabolite which delivers the acetate moiety for synthesis of acetyl-CoA, further utilised for fatty acid generation. In the mitochondrial matrix of neuronal cells, N-acetylaspartate synthetase (NAT8L) catalyses the formation of NAA from acetyl-CoA (Ac-CoA) and L-aspartatic acid (L-Asp) (Wiame et al. 2009, Pessentheiner et al. 2013, Prokesch et al. 2016).
This is catalyzed by the same transferase activity as was used previously for the original acetyl group. The butyryl group is now ready to condense with a new malonyl group (third reaction above) to repeat the process.
A common type of epigenetic modification is called DNA methylation. DNA methylation involves the attachment of small chemical groups called methyl groups (each consisting of one carbon atom and three hydrogen atoms) to DNA building blocks. When methyl groups are present on a gene, that gene is turned off or silenced, and no protein is produced from that gene.
Another common epigenetic change is histone modification. Histones are structural proteins in the cell nucleus. DNA wraps around histones, giving chromosomes their shape. Histones can be modified by the addition or removal of chemical groups, such as methyl groups or acetyl groups (each consisting of two carbon, three hydrogen, and one oxygen atoms). The chemical groups influence how tightly the DNA is wrapped around histones, which affects whether a gene can be turned on or off.
Errors in the epigenetic process, such as modification of the wrong gene or failure to add a chemical group to a particular gene or histone, can lead to abnormal gene activity or inactivity. Altered gene activity, including that caused by epigenetic errors, is a common cause of genetic disorders. Conditions such as cancers, metabolic disorders, and degenerative disorders have been found to be related to epigenetic errors.
Acetyl products ultimately supply products used by a range of end markets, from the construction industry through to the agricultural sector. A well known acetyl is polyester fibre, which is used in many of the clothes that we wear everyday. Acetyls also support a wide range of downstream industries in food flavouring and preservation, pharmaceuticals, paints, adhesives and packaging.
Increasing blood bicarbonate content has long been cited as a potential mechanism to improve contractile function. We investigated whether sodium bicarbonate-induced metabolic alkalosis could positively affect force development during the rest-to-work transition in ischaemic skeletal muscle. Secondly, assuming it could, we investigated whether bicarbonate could augment acetyl group availability through the same equilibrium reaction as sodium acetate pre-treatment and whether this underpins, at least in part, its ergogenic effect. Multiple biopsy samples were obtained from the canine gracilis muscle during 5 min of electrically evoked ischaemic contraction, which enabled the determination of the time course of acetyl group accumulation, substrate utilisation, pyruvate dehydrogenase complex activation and tension development in animals treated with saline (control; n = 6) or sodium bicarbonate (n = 5). Treatment with bicarbonate elevated acetylcarnitine content above the control level at rest (P 041b061a72