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N Acetyl Cysteine
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N Acetyl l cysteine (also spelled acetylcysteine, N Acetyl L Cysteine or N-acetylcyteine) is made from the amino acid cysteine joined to an acetyl group. Acetylcysteine (sometimes abbreviated as N-A-C or NAC) is a strong antioxidant. It donates the amino acid cysteine to help form the antioxidant glutathione. Glutathione is a powerful antioxidant normally found in the body. In hospitals, acetylcysteine is used for liver protection in cases of acetaminophen toxicity.
N Acetyl Cysteine Supplement
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N Acetyl Cysteine bBenefit
An excellent review article in the April 1998 issue of Alternative Medicine Reviews summarizes the known effects of acetylcysteine. The author writes, “N-acetylcysteine is an excellent source of sulfhydryl groups, and is converted in the body into metabolites capable of stimulating glutathione synthesis, promoting detoxification, and acting directly as a free radical scavenger. Administration of acetylcysteine has historically been as a mucolytic [mucus dissolving] agent in a variety of respiratory illnesses; however, it appears to also have beneficial effects in conditions characterized by decreased glutathione or oxidative stress, such as HIV infection, cancer, heart disease, and cigarette smoking.” N Acetylcysteine has liver protecting benefits.
Acetylcyteine may prevent toxicity to the kidneys during x-ray testing after injection with a contrast material in the bloodstream.
Patients with acute myocardial infarction undergoing primary angioplasty are at high risk for contrast-medium–induced nephropathy because of hemodynamic instability, the need for a high volume of contrast medium, and the lack of effective prophylaxis. We investigated the antioxidant N-acetylcysteine for the prevention of contrast-medium–induced nephropathy in patients undergoing primary angioplasty. We randomly assigned 354 consecutive patients undergoing primary angioplasty to one of three groups: 116 patients were assigned to a standard dose of N-acetylcysteine (a 600-mg intravenous bolus before primary angioplasty and 600 mg orally twice daily for the 48 hours after angioplasty), 119 patients to a double dose of N-acetylcysteine (a 1200-mg intravenous bolus and 1200 mg orally twice daily for the 48 hours after intervention), and 119 patients to placebo. Results The serum creatinine concentration increased 25 percent or more from baseline after primary angioplasty in 39 of the control patients (33 percent), 17 of the patients receiving standard-dose N-acetylcysteine (15 percent), and 10 patients receiving high-dose N-acetylcysteine. Overall in-hospital mortality was higher in patients with contrast-medium–induced nephropathy than in those without such nephropathy (26 percent vs. 1 percent). Thirteen patients (11 percent) in the control group died, as did five (4 percent) in the standard-dose N-acetylcysteine group and three (3 percent) in the high-dose N-acetylcysteine group. The rate for the composite end point of death, acute renal failure requiring temporary renal-replacement therapy, or the need for mechanical ventilation was 21 (18 percent), 8 (7 percent), and 6 (5 percent) in the three groups, respectively. Intravenous and oral N-acetylcysteine may prevent contrast-medium–induced nephropathy with a dose-dependent effect in patients treated with primary angioplasty and may improve hospital outcome.
N acetylcysteine benefit
for lowering homocysteine
Oral N acetylcysteine may lower homocysteine levels.
Dr. Peter W. Kalivas from the Medical University of South Carolina, Charleston evaluated the effects of N-Acetylcysteine on cue-induced cocaine craving of 15 people with cocaine dependence. Those who were taking the N-Acetylcysteine supplements had less cocaine craving and interest evoked by depictions of cocaine use on photographic slides. The neurotransmitter system involved may be glutamate transmission. Dr. Peter W. Kalivas is now starting a double-blind study is being conducted to evaluate the effect of N-Acetylcysteine on relapse rates and also evaluating the effects of N-Acetylcysteine on nicotine and marijuana craving.
Is cocaine desire reduced by N-acetylcysteine?
Am J Psychiatry. 2007 Jul;164(7):1115-7. LaRowe SD, Myrick H, Hedden S, Mardikian P, Saladin M, McRae A, Brady K, Kalivas PW, Malcolm R. Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC 29425,
In this double-blind, placebo-controlled trial, 15 volunteers received acetylcysteine or placebo during a 3-day hospitalization. Participants were crossed over to receive the opposite condition on a second, identical 3-day stay occurring 4 days later. During each hospital stay, participants completed a cue-reactivity procedure that involved collecting psychophysical and subjective data in response to slides depicting cocaine and cocaine use. While taking N-acetylcysteine, participants reported less desire to use and less interest in response to cocaine slides and watched cocaine slides for less time.
An open-label trial of N-acetylcysteine for the
treatment of cocaine dependence: a pilot study.
Prog Neuropsychopharmacol Biol Psychiatry. 2007 Mar 30;31(2):389-94. Mardikian PN, LaRowe SD, Hedden S, Kalivas PW, Malcolm RJ. Center for Drug and Alcohol Programs, Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, 67 President Street, Charleston, SC 29425, USA.
Twenty three treatment-seeking cocaine-dependent patients participated in a 4-week medication trial and received N-acetylcysteine at doses of 1200 mg/day, 2400 mg/day or 3600 mg/day. Results suggested that the three doses were well tolerated. Overall, the retention rates appeared to favor higher doses of NAC (2400 mg/day and 3600 mg/day). The majority of subjects who completed the study either terminated use of cocaine completely or significantly reduced their use of cocaine during treatment.
Benefit of n acetylcysteine
for acute respiratory distress syndrome
Patients with ARDS are in a deficient oxidant-anti-oxidant balance and can get a significant benefit if supplemented with acetylcysteine NAC.
Benefit of acetylcysteine
in cystic fibrosis
Oral N-acetylcysteine, through its actions on glutathione, may reduce inflammation in cystic fibrosis.
N Acetylcysteine side effects
Other than large doses causing nausea, acetylcysteine does not have any significant side effects and appears to be a safe nutrient as long as the dosage is kept to less than 500 mg. Nausea can occur for a few minutes within an hour of taking two or three n acetylcysteine 600 mg pills on an empty stomach.
One possible acetylcysteine side effect that should be kept in mind (it could also be an acetylcysteine benefit) is that this supplement has anticoagulant and platelet-inhibiting properties.
Regular use of the painkiller acetaminophen is associated with higher rates of asthma and chronic obstructive pulmonary disease and reduced lung function. Animal experiments have suggested that acetaminophen might lower antioxidant activity in the lungs, and causes harm to the liver and kidneys.
With hundreds of people each year dying from acetaminophen overdose, thousands more with liver damage or other health problems, why is acetaminophen still available for sale without a prescription whereas regulators have tried to pull away certain nutritional supplements that are far less toxic?
Those who need to take acetaminophen for a health condition should consider Acetylcysteine, a nutrient that protects the liver from this drug's toxicity. The antidote for acetaminophen poisoning is N acetyl cysteine. Acetylcysteine is thought to work through a number of protective mechanisms. Acetylcysteine is a precursor of glutathione and increases glutathione availability. Acetylcysteine also functions as an anti-inflammatory and antioxidant and has positive inotropic effects. Acetylcysteine increases local nitric oxide concentrations, and this vasodilatory effect on microcirculatory blood flow enhances local oxygen delivery to peripheral tissues. These vasodilating effects decrease morbidity and mortality even in the setting of established liver damage.
Doctors prescribe intravenous or IV acetylcysteine to patients with liver damage due to acetaminophen (Tylenol) overdose. Acetylcysteine IV protects the liver quite well.
Acetyl cysteine is sold in dosages ranging from 250 to 600 mg. Acetylcysteine can help form the powerful antioxidant glutathione but the formation of glutathione synthesis is under feedback control. Administration of acetylcysteine with the resulting increase in glutathione levels may cause a feedback inhibition in glutathione synthesis. Thus, it may be best to take acetylcysteine every other day. The use of acetylcysteine certainly should be considered as an additional supplement in protecting various cells from damage in the elderly and those with Parkinson’s disease. If you are planning to use acetylcysteine along with other antioxidants, limit your daily dosage to 100 to 500 mg and don’t take it all the time. Acetylcysteine could protect the liver in those who take acetaminophen on a regular basis.
N Acetylcysteine supplement
You can find oral acetylcysteine in varying dosages
N acetylcysteine 200 mg oral tablets or capsules
N acetylcysteine 250 mg oral pills
N acetylcysteine 500 mg oral pills
N acetylcysteine 600 mg oral pills - unless you are being treated for a medical condition, there is no reason to take n acetylcysteine 600 mg tablets or capsules on a daily basis.
What is the ideal daily n
There are no strict guidelines on the best acetylcysteine dose to take daily. It may be a good idea to limit the use of acetylcysteine supplements to two or three times a week rather than daily unless your doctor has prescribed this supplement as a treatment for a medical condition.
N acetylcysteine side effects
Oral overdosage of acetylcysteine could result in side effects such as nausea, vomiting and other gastrointestinal symptoms. Rare acetylcysteine side effects could include bronchospasm.
Acetylcysteine Research and
Thiolic antioxidant supplementation of the diet reverses age-related behavioural dysfunction in prematurely ageing mice.
Pharmacol Biochem Behav. 2005 Jan;80(1):45-51.
We have studied in a model of premature ageing in mice based on their impaired behavioural response in a simple T-maze test the effect of the ingestion of thioproline (TP) plus N-acetylcysteine (0.1% w/w of each antioxidant) by female and male mice of Swiss and BALB/c strains on performance in two behaviour tests. The antioxidant treatment (4 weeks in two different periods of life, i.e., adult and old age) protected all animals against early-age-associated behavioural impairment, but this improvement was more evident in the prematurely ageing mice (PAM) in comparison to the control group or non-prematurely ageing mice (NPAM). These effects could be due to the glutathione precursor role of acetylcysteine and thioproline that replenish the intracellular reduced glutathione (GSH) levels despite advancing age. In conclusion, diet supplementation with acetylcysteine and thioproline appears to be an effective therapy for protection against early behavioural decline in prematurely ageing mice.
A patient-tailored N-acetylcysteine protocol for acute acetaminophen
Clin Ther. 2005 Mar;27(3):336-41.
Hepatotoxicity as a result of acetaminophen (APAP) intoxication has become an important problem, but early intervention with N-acetylcysteine (Acetylcysteine) is effective in preventing hepatic injury. Two Acetylcysteine regimens are currently approved for acute APAP intoxication: Acetylcysteine administered orally every 4 hours for 72 hours, and Acetyl cysteine administered intravenously for 20 hours within 8 to 10 hours after ingestion of a potentially hepatotoxic amount of APAP. However, clinical observations suggest that a variable treatment duration may be more appropriate than use of these predetermined, fixed-duration protocols. This study investigated the tolerability and efficacy of a patient-tailored N Acetylcysteine protocol for acute APAP intoxication by comparing the incidence of hepatotoxicity in patients receiving this protocol and in historical controls receiving 1 of 2 fixed-duration protocols: oral Acetylcysteine for 72 hours and intravenous Acetylcysteine for 20 hours within 8 to 10 hours after ingestion of a potentially hepatotoxic amount of APAP. This was a retrospective case series study that included all patients admitted through the emergency department (ED) of the National Taiwan University Hospital with a diagnosis of APAP intoxication between October 1997 and October 2002. According to the patient-tailored protocol, which had been used in the ED since 1997, patients with a serum APAP concentration above the limit for possible risk based on a modified Rumack-Matthew nomogram received oral treatment with Acetylcysteine 140 mg/kg, followed by maintenance doses of 70 mg/kg every 4 hours. Acetylcysteine treatment was discontinued when the APAP concentration was <10 mg/L and serum aspartate aminotransferase (AST) was <40 IU/L. For the purposes of assessing clinical outcomes, patients were divided into 3 groups based on duration of treatment: the short-course group (</=36 hours), the intermediate-course group (37-72 hours), and the long-course group (>/=73 hours). The primary outcome measure was development of hepatotoxicity, defined as a serum AST or alanine aminotransferase concentration >1000 IU/L. Twenty-seven patients were included in the study, 17 in the short-course group, 4 in the intermediate-course group, and 6 in the long-course group. The mean (SD) durations of Acetyl l cysteine treatment in the respective groups were 22.1 (5.5) hours, 45.0 (8.2) hours, and 97 (33) hours. All 6 patients (22%) in the long-course group had hepatotoxicity (peak AST range, 1083-9770 IU/L); their treatment duration ranged from 80 to 164 hours. No patients in the short- or intermediate-course group had evidence of hepatotoxicity. One woman in the long-course group in whom initiation of Acetylcysteine treatment was delayed by 28 hours died of fulminant hepatic failure. The overall incidence of hepatotoxicity was similar to that in the historical controls. In this retrospective case series inpatients who received patient-tailored Acetylcysteine therapy for acute APAP intoxication, the incidence of hepatotoxicity was low and comparable to that in historical controls who received treatment with 1 of 2 fixed-duration regimens. Use of this protocol may have the potential to shorten hospital stays without increasing the risk to patients. However, the sample size was small, and the findings require confirmation in prospective clinical trials.
Effect of dietary restriction and n acetyl cysteine supplementation on
intestinal mucosa and liver mitochondrial redox status and function in
Exp Gerontol. 2004 Sep;39(9):1323-32.
The age-related changes of glutathione (GSH) levels and the effect of hypocaloric regimen and acetylcysteine supplementation were investigated in intestinal mucosa and liver mitochondria of 28 months rats. Old rats exhibited lower proteins, GSH and protein sulphydrils concentrations, higher GSH-peroxidase (GSH-Px) activity and protein carbonyl deposit, partial inhibition of succinate stimulated mitochondrial state III respiration and decreased mitochondrial nitrosothiols concentration. In conclusion, ageing is characterized by a decrease of GSH concentrations, increased protein oxidation and decreased mitochondrial NO content. Hypocaloric diet ameliorated intestinal transport and, as well as acetylcysteine, was effective in enhancing GSH levels but at different extent according to the investigated districts. Both interventions reduced the age-associated increase of GSH-Px and protein carbonyls and improved mitochondrial respiration.
Treatment by acetylcysteine and melatonin
increases cardiac baroreflex and improves antioxidant reserve.
Am J Hypertens. 2004 Oct;17(10):947-54.
The aims of this study were to investigate the effects of melatonin and acetylcysteine on the baroreflex sensitivity and to verify whether those effects were correlated with their antioxidant capacity in Wistar-Kyoto and spontaneously hypertensive rats (SHR). Rats were treated with 30 mg/kg/day of melatonin or 4 g/kg/day of acetylcysteine for 4 weeks. Changes in mean arterial pressure, heart rate, plasma norepinephrine, and epinephrine were measured in conscious rats after an intravenous injection of phenylephrine or sodium nitroprusside. RESULTS: Melatonin and acetylcysteine produced a significant reduction in mean arterial pressure and heart rate in SHR. Melatonin and acetylcysteine improved bradycardic and tachycardic baroreflex responses in SHR without modifying catecholamine responses. The antioxidant reserve, which was reduced in SHR as reflected by the lower glutathione peroxidase activity in plasma, was normalized by acetylcysteine and melatonin. Acetylcysteine and melatonin increased glutathione peroxidase activity in erythrocytes from SHR. The results of the present study suggest that melatonin and acetylcysteine improve the baroreflex response in SHR in correlation with the antioxidant effects of these substances.
N Acetyl cysteine in nephrology; contrast nephropathy
Curr Opin Nephrol Hypertens. 2004 Nov;13(6):649-54.
Since the first publication appeared in 2000 showing that prophylactic oral administration of the antioxidant acetylcysteine, along with adequate hydration, can prevent the reduction in renal function induced by non-ionic, low-osmolality contrast agents, acetylcysteine has rapidly become widely used in clinical practice. Meanwhile, other applications of acetylcysteine in nephrology have been reported. This review analyses recent literature on the effects of acetylcysteine on radiocontrast-induced nephropathy, on plasma homocysteine concentrations, and on cardiovascular events in patients with end-stage renal failure. At least 19 randomized trials evaluating acetylcysteine for the prevention of radiocontrast-induced nephropathy, at least five meta-analyses, and several reviews on that topic have been published within the past 4 years. One study recently indicated that the administration of acetylcysteine during a haemodialysis session significantly lowered plasma homocysteine concentrations. Another study indicated that long-term antioxidative treatment with acetylcysteine significantly reduced cardiovascular events in patients with end-stage renal failure. Although there are controversies on dosing and timing, the use of acetylcysteine together with hydration should be considered to protect patients from radiographic contrast media-induced nephropathy. Long-term antioxidative treatment with acetylcysteine in patients with end-stage renal failure may also be useful to prevent adverse cardiovascular events.
Protective effect of n acetyl cysteine and deferoxamine on carbon tetrachloride-induced acute hepatic failure in rats.
Crit Care Med. 2004 Oct;32(10):2079-2083.
Carbon tetrachloride (CCl4) is a lipid-soluble potent hepatotoxic; thus, it widely is used as an animal model of severe hepatic failure. We here describe the effects of acetylcysteine, deferoxamine, or both in the treatment of CCl4-induced hepatic failure. Rats exposed to CCl4 were treated with acetylcysteine and/or deferoxamine or vehicle. Acetylcysteine plus deferoxamine treatment significantly attenuated hepatic and central nervous system oxidative damage after acute hepatic failure induced by CCl4. In addition, the serum levels of alanine aminotransferase, total bilirubin, and prothrombin time in the acetylcysteine plus deferoxamine group were significantly lower than those in the acetylcysteine or deferoxamine and saline groups. After acetylcysteine plus deferoxamine treatment, hepatocellular necrosis and inflammatory infiltration induced by carbon tetrachloride were greatly decreased. Survival in untreated rats was 5%. Survival increased to 25% and 35%, respectively, with acetylcysteine and deferoxamine treatment. In rats treated with acetylcysteine plus deferoxamine, survival was 80%. Our data provide the first experimental demonstration that acetylcysteine plus deferoxamine reduces mortality rate, decreases oxidative stress, and limits inflammatory infiltration and hepatocyte necrosis induced by CCl4 in the rat.
N acetyl cysteine
prevents cisplatin-induced ototoxicity in rats
Hearing Res 2004;July issue.
Treatment with acetylcysteine can prevent the ototoxic effects often seen with cisplatin therapy. In the current study, reported in the July issue of Hearing Research, the researchers tested the benefits of acetylcysteine treatment in a newly developed rat model of cisplatin-induced ototoxicity. Animals were treated with acetylcysteine or saline 15 or 30 minutes before receiving cisplatin or 4 hours afterward. The acetylcysteine-treated rats showed no significant change in auditory brainstem response with cisplatin therapy. In contrast, the saline-treated animals displayed marked ototoxicity.
Counteracting Tylenol Toxicity
In addition to its antioxidant properties, acetylcysteine is currently used in a variety of other ways: to counteract the effects of an overdose of acetaminophen (i.e., Tylenol®), to break up mucus in respiratory ailments, to lessen the symptoms of colds or the flu, and even to reduce the effects of hangovers.
Regular use of the painkiller acetaminophen is associated with higher rates of liver and kidney toxicity, asthma, and chronic obstructive pulmonary disease and reduced lung function.
My comments: With hundreds of people each year dying from acetaminophen overdose, thousands more with liver damage or other health problems, why is acetaminophen still available for sale without a prescription whereas regulators have tried to pull away certain nutritional supplements that are far less toxic?
Those who need to take acetaminophen for a health condition should consider acetylcysteine, a nutrient that protects the liver from this drug's toxicity.
Acetylcysteine and Cocaine
A study funded by the National Institutes of Health (NIH) suggests that acetylcysteine can reduce the cravings associated with chronic cocaine use. This research, released at the American College of Neuropsychopharmacology's (ACNP) annual conference is among the first to identify N-acetylcysteine (NAC) as a potential agent to modulate the effects of cocaine addiction. There is also early evidence in animal models of addiction to suggest that this chemical works similarly in the treatment of heroin addiction, and possibly alcoholism. NAC is available over the counter as an herbal supplement known for its antioxidant effects. In the first phase of the study, the research team conditioned rats on a regimen of cocaine to establish their addiction. The rats in the treatment group were then treated with N acetylcysteine. After treatment, the cocaine-addicted rats exposed to N-acetylcysteine were significantly less likely to seek out cocaine than those without N acetylcysteine. Those treated with NAC ceased to actively seek cocaine, but showed normal food-seeking behaviors.
In the second phase of the study, acetylcysteine treatment was investigated in a small inpatient study (n=15) involving non-treatment seeking cocaine-dependent subjects. In this phase of research, subjects were asked to look at pictures that were either neutral (e.g., trees, boats) or cocaine-related (e.g., drug paraphernalia). Those individuals treated with N-acetylcysteine reported less craving for cocaine and spent less time looking at the cocaine-related pictures. In addition, when using a functional magnetic resonance imaging test, subjects treated with acetylcysteine had reduced brain activity in the prefrontal cortex, the area of the brain activated during cocaine craving and used to modulate the addictive behavior of chronic cocaine use. An open label trial, which was recently completed, indicated that cocaine-dependent patients could take N-acetyl cysteine on an extended outpatient basis, with minimal side effects. More importantly, patients taking higher doses of NAC were more likely to complete the trial, providing further indication of the potential benefits of N-acetylcysteine.
N Acetyl Cystiene emails
Q. I was wondering if I could "overdose" on NAC. What is the safest maximum per-day dosage??
A. Each person has a different threshold for N acetyl cysteine, but as with most supplements, more is not better, there could be a feedback loop, or tolerance, or displacement of other crucial nutrients, etc. I personally prefer not to exceed 250 mg of acetylcysteine a few times a week, but a different doctor may have a different opinion.
Q. Hi, what exactly is the difference between
Cysteine and N Acetyl cysteine ? Which one is better to take?
A. Most often, aceytylcysteine is the one taken since it has stronger antioxidant potential, however it depends on the condition being treated. Acetylcysteine has an additional acetyl group which makes it more potent as an antioxidant.
Q. What is the right n acetylcysteine dosage as a
A. There are no accepted guidelines on the appropriate n acetylcysteine daily dosage. Some people may need none, others may benefit from taking 500 mg of n acetylcysteine a few days a week. If you are taking other antioxidants, we suggest you reduce your dosage of n acetylcysteine. Some people think that the more antioxidants they take the healthier they will be, but there is no proof of this.
Q. Should one take n acetyl l cysteine if they are taking Tylenol (acetaminophen) ? I understand that acetaminophen can damage the liver and n acetylcysteine can protect the liver from Tylenol harm.
A. This is a good question. If your doctor approves, it may be a good idea to take a small daily amount or a few times a week of a n acetylcysteine supplement, although there is little research to guide us on how much is needed and how often one should take the acetylcysteine.
Q. I would like to use acetylcysteine to protect my
liver from the amount of acetaminophin I am required to take on a daily
basis due to my injuries. How much would I need to take of acetylcysteine?
A. We have not seen any studies regarding the long term use of acetaminophen and acetylcysteine, however a dose of 100 mg a day would seem reasonable.
Q. I bought n acetylcysteine tablets at 600mg, is it
okay to break these tablets in two pieces and take half a tablet two or
three times a week?
A. Yes, it is okay to take half a tablet of acetylcysteine 600 mg.