Acetylcysteine

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Acetylcysteine
Acetylcysteine2.svg
Acetylcysteine-from-xtal-3D-bs-17.png
Clinical data
Pronunciation /əˌsiːtəlˈsɪstiːn/ and similar ( /əˌsɛtəl-,ˌæsɪtəl-,-tiːn/ )
Trade names ACC 200, Acetadote, Fluimucil, Mucomyst, others
Other namesN-acetylcysteine; N-acetyl-L-cysteine; NALC; NAC
AHFS/Drugs.com Monograph
License data
Pregnancy
category
  • AU:B2
Routes of
administration 		oral, intravenous, inhalation
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability 6–10% (Oral) [6] [7]
nearly 100% (intravenous) [8]
Protein binding 50 to 83% [9]
Metabolism Liver [9]
Elimination half-life 5.6 hours [5]
Excretion Kidney (30%), [9] faecal (3%)
Identifiers
  • (2R)-2-acetamido-3-sulfanylpropanoic acid [10]
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard 100.009.545 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C5H9NO3S
Molar mass 163.19 g·mol−1
3D model (JSmol)
Specific rotation +5° (c = 3% in water) [11]
Melting point 109 to 110 °C (228 to 230 °F) [11]
  • C/C(=N/[C@@H](CS)C(=O)O)/O
  • InChI=1S/C5H9NO3S/c1-3(7)6-4(2-10)5(8)9/h4,10H,2H2,1H3,(H,6,7)(H,8,9)/t4-/m0/s1 Yes check.svgY
  • Key:PWKSKIMOESPYIA-BYPYZUCNSA-N Yes check.svgY
   (verify)

N-acetylcysteine, also known as Acetylcysteine and NAC, is a medication that is used to treat paracetamol (acetaminophen) overdose and to loosen thick mucus in individuals with chronic bronchopulmonary disorders, such as pneumonia and bronchitis. [9] It has been used to treat lactobezoar in infants. It can be taken intravenously, orally (swallowed by mouth), or inhaled as a mist. [9] [ clarification needed ] It is also sometimes used as a dietary supplement. [12] [13]

Contents

Common side effects include nausea and vomiting when taken orally. [9] The skin may occasionally become red and itchy with any route of administration. [9] A non-immune type of anaphylaxis may also occur. [9] It appears to be safe in pregnancy. [9] For paracetamol overdose, it works by increasing the level of glutathione, an antioxidant that can neutralize the toxic breakdown products of paracetamol. [9] When inhaled, it acts as a mucolytic by decreasing the thickness of mucus. [14]

Acetylcysteine was initially patented in 1960 and came into medical use in 1968. [15] [16] [17] It is on the World Health Organization's List of Essential Medicines. [18] [19] It is available as a generic medication. [20]

The sulfur-containing amino acids cysteine and methionine are more easily oxidized than the other amino acids. [21] [22]

Uses

Medical uses

Paracetamol overdose antidote

Intravenous and oral formulations of acetylcysteine are available for the treatment of paracetamol (acetaminophen) overdose. [23] When paracetamol is taken in large quantities, a minor metabolite called N-acetyl-p-benzoquinone imine (NAPQI) accumulates within the body. It is normally conjugated by glutathione, but when taken in excess, the body's glutathione reserves are not sufficient to deactivate the toxic NAPQI. This metabolite is then free to react with key hepatic enzymes, thereby damaging liver cells. This may lead to severe liver damage and even death by acute liver failure.

In the treatment of paracetamol (acetaminophen) overdose, acetylcysteine acts to maintain or replenish depleted glutathione reserves in the liver and enhance non-toxic metabolism of acetaminophen. [24] These actions serve to protect liver cells from NAPQI toxicity. It is most effective in preventing or lessening hepatic injury when administered within 8–10 hours after overdose. [24] Research suggests that the rate of liver toxicity is approximately 3% when acetylcysteine is administered within 10 hours of overdose. [23]

Although IV and oral acetylcysteine are equally effective for this indication, oral administration is generally poorly tolerated due to the higher dosing required to overcome its low oral bioavailability, [25] its foul taste and odour, and a higher incidence of adverse effects when taken orally, particularly nausea and vomiting. Prior pharmacokinetic studies of acetylcysteine did not consider acetylation as a reason for the low bioavailability of acetylcysteine. [26] Oral acetylcysteine is identical in bioavailability to cysteine precursors. [26] However, 3% to 6% of people given intravenous acetylcysteine show a severe, anaphylaxis-like allergic reaction, which may include extreme breathing difficulty (due to bronchospasm), a decrease in blood pressure, rash, angioedema, and sometimes also nausea and vomiting. [27] Repeated doses of intravenous acetylcysteine will cause these allergic reactions to progressively worsen in these people.

Several studies have found this anaphylaxis-like reaction to occur more often in people given intravenous acetylcysteine despite serum levels of paracetamol not high enough to be considered toxic. [28] [29] [30] [31]

Mucolytic agent

Acetylcysteine exhibits mucolytic properties, meaning it reduces the viscosity and adhesiveness of mucus. This therapeutic effect is achieved through the cleavage of disulfide bonds [32] within mucoproteins (strongly cross-linked mucins), [33] thereby decreasing the mucus viscosity and facilitating its clearance from the respiratory tract. This mechanism is particularly beneficial in conditions characterized by excessive or thickened mucus, [34] such as chronic obstructive pulmonary disease (COPD), cystic fibrosis, rhinitis or sinusitis. [35] Acetylcysteine can be administered as a part of a complex molecule, Thiamphenicol glycinate acetylcysteine, which also contains thiamphenicol, an antibiotic. [36]

Lungs

Inhaled acetylcysteine has been used for mucolytic therapy in addition to other therapies in respiratory conditions with excessive and/or thick mucus production. It is also used post-operatively, as a diagnostic aid, and in tracheotomy care. It may be considered ineffective in cystic fibrosis. [37] A 2013 Cochrane review in cystic fibrosis found no evidence of benefit. [38]

Acetylcysteine is used in the treatment of obstructive lung disease as an adjuvant treatment. [39] [40] [41]

Other uses

Acetylcysteine has been used to complex palladium, to help it dissolve in water. This helps to remove palladium from drugs or precursors synthesized by palladium-catalyzed coupling reactions. [42] N-acetylcysteine can be used to protect the liver. [43]

Microbiological use

Acetylcysteine can be used in Petroff's method of liquefaction and decontamination of sputum, in preparation for recovery of mycobacterium. [44] It also displays significant antiviral activity against influenza A viruses. [45]

Acetylcysteine has bactericidal properties and breaks down bacterial biofilms of clinically relevant pathogens including Pseudomonas aeruginosa , Staphylococcus aureus , Enterococcus faecalis , Enterobacter cloacae , Staphylococcus epidermidis , and Klebsiella pneumoniae . [46]

Side effects

The most commonly reported adverse effects for IV formulations of acetylcysteine are rash, urticaria, and itchiness. [24]

Adverse effects for inhalational formulations of acetylcysteine include nausea, vomiting, stomatitis, fever, rhinorrhea, drowsiness, clamminess, chest tightness, and bronchoconstriction. Although infrequent, bronchospasm has been reported to occur unpredictably in some patients. [47]

Adverse effects for oral formulations of acetylcysteine have been reported to include nausea, vomiting, rash, and fever. [47]

Large doses in a mouse model showed that acetylcysteine could potentially cause damage to the heart and lungs. [48] They found that acetylcysteine was metabolized to S-nitroso-N-acetylcysteine (SNOAC), which increased blood pressure in the lungs and right ventricle of the heart (pulmonary artery hypertension) in mice treated with acetylcysteine. The effect was similar to that observed following a 3-week exposure to an oxygen-deprived environment (chronic hypoxia). The authors also found that SNOAC induced a hypoxia-like response in the expression of several important genes both in vitro and in vivo . The implications of these findings for long-term treatment with acetylcysteine have not yet been investigated. The dose used by Palmer and colleagues was dramatically higher than that used in humans, the equivalent of about 20 grams per day. [48] In humans, a much lower dosages (600 mg per day) have been observed to counteract some age-related decline in the hypoxic ventilatory response as tested by inducing prolonged hypoxia. [49]

Although N-acetylcysteine prevented liver damage in mice when taken before alcohol, when taken four hours after alcohol it made liver damage worse in a dose-dependent fashion. [50]

Pharmacology

Pharmacodynamics

Acetylcysteine serves as a prodrug to L-cysteine, a precursor to the biologic antioxidant glutathione. Hence administration of acetylcysteine replenishes glutathione stores. [51]

L-cysteine also serves as a precursor to cystine, which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes; hence there is increasing glutamate release into the extracellular space. This glutamate in turn acts on mGluR2/3 receptors, and at higher doses of acetylcysteine, mGluR5. [57] [58] Acetylcysteine may have other biological functions in the brain, such as the modulation of dopamine release and the reduction in inflammatory cytokine formation possibly via inhibiting NF-κB and modulating cytokine synthesis. [55] These properties, along with the reduction of oxidative stress and the re-establishment of glutamatergic balance, would lead to an increase in growth factors, such as brain-derived neurotrophic factor (BDNF), and the regulation of neuronal cell death through B-cell lymphoma 2 expression (BLC-2). [59]

Pharmacokinetics

The oral bioavailability of acetylcysteine is relatively low due to extensive first-pass metabolism in the gut wall and liver. It ranges between 6% and 10%.

Intravenous administration of acetylcysteine bypasses the first-pass metabolism, resulting in higher bioavailability compared to oral administration. Intravenous administration of acetylcysteine ensures nearly 100% bioavailability as it directly enters the bloodstream.

Acetylcysteine is extensively liver metabolized, CYP450 minimal, urine excretion is 22–30% with a half-life of 5.6 hours in adults and 11 hours in newborns.[ medical citation needed ]

Acetylcysteine is the N-acetyl derivative of the amino acid L-cysteine, and is a precursor in the formation of the antioxidant glutathione in the body. The thiol (sulfhydryl) group confers antioxidant effects and is able to reduce free radicals.

Chemistry

Pure acetylcysteine is in a solid state at room temperature, appearing as a white crystalline powder or granules. [60] The solid form of acetylcysteine is stable under normal conditions, but it can undergo oxidation if exposed to air or moisture over time, leading to the formation of its dimeric form, diacetylcysteine, which can have different properties. [61] Acetylcysteine is highly hygroscopic, i.e., it absorbs moisture if exposed to open air. [60]

Acetylcysteine can sometimes appear as a light yellow cast powder instead of pure white due to oxidation. The sulfur-containing amino acids, like cysteine, are more easily oxidized than other amino acids. When exposed to air or moisture, acetylcysteine can oxidize, leading to a slight yellowish tint. [60]

Pure acetylcysteine is in a solid state at room temperature, appearing as a white crystalline powder or granules. The solid form of acetylcysteine is stable under normal conditions, but it can undergo oxidation if exposed to air or moisture over time, leading to the formation of its dimeric form, diacetylcysteine, which can have different properties. Acetylcysteine is highly hygroscopic, i.e., it absorbs moisture if exposed to open air. [60]

Acetylcysteine in a form of a white or white with light yellow cast powder has a pKa of 9.5 at 30 °C. [11]

N-acetyl-L-cysteine is soluble in water and alcohol, and practically insoluble in chloroform and ether. [62]

Acetylcysteine is highly soluble in water: it dissolves readily in water, forming a clear solution. The pH of a maximum-saturated acetylcysteine solution typically ranges between 6.0 and 7.5, [63] depending on temperature, purity of the compount, presense of other ions (thet can affect the pH by interacting with acetylcysteine or altering the overall ionic strength of the solution), thus on the concentraton of acetylcysteine itself: higher concentrations of acetylcysteine can lead to a lower pH due to the increased presence of the acetylcysteine molecule itself. This range of pH between 6.0 and 7.5 ensures that the solution is neither too acidic nor too alkaline, making it suitable for various medical applications. Aqueous solutions of acetylcysteine are compatible with 0.9% sodium chloride solution; compatibility with 5% and 10% glucose solutions is also good. [60]

As for the sunlight stability, acetylcysteine in dry powder form is relatively stable and does not degrade quickly when exposed to sunlight, but hen dissolved in aqueus solution, acetylcysteine can degrade when exposed to sunlight, especially if the solution is not stored in a dark, cool place. Besides that, acetylcysteine in aqueous solution can undergo hydrolysis, leading to the breakdown of the amide bond in the molecule. Still, aqueous solutions of acetylcysteine are generally stable when stored properly: the solutions should be kept in tightly sealed containers and stored at controlled room temperature to prolong the stability. [64] [60]

Society and culture

Acetylcysteine was first studied as a drug in 1963. Amazon removed acetylcysteine for sale in the US in 2021, due to claims by the FDA of it being classified as a drug rather than a supplement. [65] [66] [67] [68] In April 2022, the FDA released draft guidance on FDA's policy regarding products labeled as dietary supplements that contain N-acetyl-L-cysteine. [69] Amazon subsequently re-listed NAC products as of August 2022. [70]

Research

While many antioxidants have been researched to treat a large number of diseases by reducing the negative effect of oxidative stress, acetylcysteine is one of the few that has yielded promising results, and is currently already approved for the treatment of paracetamol overdose. [71]

Kidney and bladder

N-acetylcysteine has been widely believed to prevent adverse effects of long term Ketamine on the bladder and kidneys, and there is growing body of evidence to support this. [86]

Evidence for the benefit of acetylcysteine to prevent radiocontrast induced kidney disease is mixed. [87]

Acetylcysteine has been used for cyclophosphamide-induced haemorrhagic cystitis, although mesna is generally preferred due to the ability of acetylcysteine to diminish the effectiveness of cyclophosphamide. [88]

Psychiatry

Acetylcysteine has been studied for major psychiatric disorders, [89] [59] [55] [73] including bipolar disorder, [89] major depressive disorder, and schizophrenia. [59] [55]

Tentative evidence exists for N-acetylcysteine also in the treatment of Alzheimer's disease, autism, obsessive-compulsive disorder, [90] specific drug addictions (cocaine), drug-induced neuropathy, trichotillomania, excoriation disorder, and a certain form of epilepsy (progressive myoclonic). [59] [55] [91] Preliminary evidence showed efficacy in anxiety disorder, attention deficit hyperactivity disorder and mild traumatic brain injury although confirmatory studies are required. [91] [92] [93] [94] Tentative evidence also supports use in cannabis use disorder. [95]

It is also being studied for use as a treatment of body-focused repetitive behavior. [96] [97]

Addiction

Evidence to date does not support the efficacy for N-acetylcysteine in treating addictions to gambling, methamphetamine, or nicotine. [91] Based upon limited evidence, NAC appears to normalize glutamate neurotransmission in the nucleus accumbens and other brain structures, in part by upregulating the expression of excitatory amino acid transporter 2 (EAAT2), a.k.a. glutamate transporter 1 (GLT1), in individuals with addiction. [82] While NAC has been demonstrated to modulate glutamate neurotransmission in adult humans who are addicted to cocaine, NAC does not appear to modulate glutamate neurotransmission in healthy adult humans. [82] NAC has been hypothesized to exert beneficial effects through its modulation of glutamate and dopamine neurotransmission as well as its antioxidant properties. [55]

Bipolar disorder

In bipolar disorder, N-acetylcysteine has been repurposed as an augmentation strategy for depressive episodes in light of the possible role of inflammation in the pathogenesis of mood disorders. Nonetheless, meta-analytic evidence shows that add-on N-acetylcysteine was more effective than placebo only in reducing depression scales scores (low quality evidence), without positive effects on response and remission outcomes, limiting its possible role in clinical practice to date. [89] [98]

COVID-19

Acetylcysteine has been studied as a possible treatment for COVID-19. [99] [100] [101]

A combination of guanfacine and N-acetylcysteine has been found to lift the "brain fog" of eight patients with long COVID, according to researchers. [102]

A combination of glycine and N-acetylcysteine is suspected to have potential to safely replenish depleted glutathione levels in COVID-19 patients. [103]

Related Research Articles

<span class="mw-page-title-main">Cysteine</span> Proteinogenic amino acid

Cysteine is a semiessential proteinogenic amino acid with the formula HOOC−CH(−NH2)−CH2−SH. The thiol side chain in cysteine often participates in enzymatic reactions as a nucleophile. Cysteine is chiral, but both D and L-cysteine are found in nature. L‑Cysteine is a protein monomer in all biota, and D-cysteine acts as a signaling molecule in mammalian nervous systems. Cysteine is named after its discovery in urine, which comes from the urinary bladder or cyst, from Greek κύστη kýsti, "bladder".

<span class="mw-page-title-main">Glutamine</span> Chemical compound

Glutamine is an α-amino acid that is used in the biosynthesis of proteins. Its side chain is similar to that of glutamic acid, except the carboxylic acid group is replaced by an amide. It is classified as a charge-neutral, polar amino acid. It is non-essential and conditionally essential in humans, meaning the body can usually synthesize sufficient amounts of it, but in some instances of stress, the body's demand for glutamine increases, and glutamine must be obtained from the diet. It is encoded by the codons CAA and CAG. It is named after glutamic acid, which in turn is named after its discovery in cereal proteins, gluten.

<span class="mw-page-title-main">Glutathione</span> Ubiquitous antioxidant compound in living organisms

Glutathione is an organic compound with the chemical formula HOCOCH(NH2)CH2CH2CONHCH(CH2SH)CONHCH2COOH. It is an antioxidant in plants, animals, fungi, and some bacteria and archaea. Glutathione is capable of preventing damage to important cellular components caused by sources such as reactive oxygen species, free radicals, peroxides, lipid peroxides, and heavy metals. It is a tripeptide with a gamma peptide linkage between the carboxyl group of the glutamate side chain and cysteine. The carboxyl group of the cysteine residue is attached by normal peptide linkage to glycine.

<span class="mw-page-title-main">Paracetamol</span> Common medication for pain and fever

Paracetamol (acetaminophen) is a non-opioid analgesic and antipyretic agent used to treat fever and mild to moderate pain. It is a widely used over-the-counter medication. Common brand names include Tylenol and Panadol.

<span class="mw-page-title-main">Acetaldehyde dehydrogenase</span> Class of enzymes

Acetaldehyde dehydrogenases are dehydrogenase enzymes which catalyze the conversion of acetaldehyde into acetyl-CoA. This can be summarized as follows:

<span class="mw-page-title-main">Pyroglutamic acid</span> Chemical compound

Pyroglutamic acid is a ubiquitous but understudied natural amino acid derivative in which the free amino group of glutamic acid or glutamine cyclizes to form a lactam. The names of pyroglutamic acid conjugate base, anion, salts, and esters are pyroglutamate, 5-oxoprolinate, or pidolate.

<span class="mw-page-title-main">Riluzole</span> Medication used to treat amyotrophic lateral sclerosis

Riluzole is a medication used to treat amyotrophic lateral sclerosis and other motor neuron diseases. Riluzole delays the onset of ventilator-dependence or tracheostomy in some people and may increase survival by two to three months. Riluzole is available in tablet and liquid form.

<span class="mw-page-title-main">Neuroprotection</span> Relative preservation of neurons

Neuroprotection refers to the relative preservation of neuronal structure and/or function. In the case of an ongoing insult the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation.

Chronic liver disease in the clinical context is a disease process of the liver that involves a process of progressive destruction and regeneration of the liver parenchyma leading to fibrosis and cirrhosis. "Chronic liver disease" refers to disease of the liver which lasts over a period of six months. It consists of a wide range of liver pathologies which include inflammation, liver cirrhosis, and hepatocellular carcinoma. The entire spectrum need not be experienced.

<i>N</i>-Acetylglutamate synthase Class of enzymes

N-Acetylglutamate synthase (NAGS) is an enzyme that catalyses the production of N-acetylglutamate (NAG) from glutamate and acetyl-CoA.

<span class="mw-page-title-main">NAPQI</span> Toxic byproduct of acetaminophen

NAPQI, also known as NAPBQI or N-acetyl-p-benzoquinone imine, is a toxic byproduct produced during the xenobiotic metabolism of the analgesic paracetamol (acetaminophen). It is normally produced only in small amounts, and then almost immediately detoxified in the liver.

<span class="mw-page-title-main">Glutathione synthetase</span> Enzyme

Glutathione synthetase (GSS) is the second enzyme in the glutathione (GSH) biosynthesis pathway. It catalyses the condensation of gamma-glutamylcysteine and glycine, to form glutathione. Glutathione synthetase is also a potent antioxidant. It is found in many species including bacteria, yeast, mammals, and plants.

<span class="mw-page-title-main">Quisqualic acid</span> Chemical compound

Quisqualic acid is an agonist of the AMPA, kainate, and group I metabotropic glutamate receptors. It is one of the most potent AMPA receptor agonists known. It causes excitotoxicity and is used in neuroscience to selectively destroy neurons in the brain or spinal cord. Quisqualic acid occurs naturally in the seeds of Quisqualis species.

<span class="mw-page-title-main">Bucillamine</span> Chemical compound

Bucillamine is an antirheumatic agent developed from tiopronin. Activity is mediated by the two thiol groups that the molecule contains. Research done in USA showed positive transplant preservation properties. Bucillamine is currently being investigated for COVID-19 drug repurposing.

Glutamate–cysteine ligase (GCL) EC 6.3.2.2), previously known as γ-glutamylcysteine synthetase (GCS), is the first enzyme of the cellular glutathione (GSH) biosynthetic pathway that catalyzes the chemical reaction:

<span class="mw-page-title-main">Excitatory amino acid transporter 3</span> Protein found in humans

Excitatory amino acid transporter 3 (EAAT3), is a protein that in humans is encoded by the SLC1A1 gene.

<span class="mw-page-title-main">Cystine/glutamate transporter</span> Protein found in humans

Cystine/glutamate transporter is an antiporter that in humans is encoded by the SLC7A11 gene.

γ-<small>L</small>-Glutamyl-<small>L</small>-cysteine Chemical compound

γ-L-Glutamyl-L-cysteine, also known as γ-glutamylcysteine (GGC), is a dipeptide found in animals, plants, fungi, some bacteria, and archaea. It has a relatively unusual γ-bond between the constituent amino acids, L-glutamic acid and L-cysteine and is a key intermediate in the γ-glutamyl cycle first described by Meister in the 1970s. It is the most immediate precursor to the antioxidant glutathione.

<span class="mw-page-title-main">Paracetamol poisoning</span> Toxicity due to paracetamol overdose

Paracetamol poisoning, also known as acetaminophen poisoning, is caused by excessive use of the medication paracetamol (acetaminophen). Most people have few or non-specific symptoms in the first 24 hours following overdose. These symptoms include feeling tired, abdominal pain, or nausea. This is typically followed by absence of symptoms for a couple of days, after which yellowish skin, blood clotting problems, and confusion occurs as a result of liver failure. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis. If death does not occur, people tend to recover fully over a couple of weeks. Without treatment, death from toxicity occurs 4 to 18 days later.

<span class="mw-page-title-main">Acetylcarnosine</span> Chemical compound

N-Acetylcarnosine (NAC) is a naturally occurring compound chemically related to the dipeptide carnosine. The NAC molecular structure is identical to carnosine with the exception that it carries an additional acetyl group. The acetylation makes NAC more resistant to degradation by carnosinase, an enzyme that breaks down carnosine to its constituent amino acids, beta-alanine and histidine.

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