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Effect of N  Acetyl Cysteine on Wound Healing

Effect of N Acetyl Cysteine on Wound Healing

N- acetyl cysteine was evaluated for its wound healing activity in ether anaesthetized albino rats by using incision, excision wound models. Significant increase in skin breaking strength, granuloma breaking strength, wound contraction and decreased in epithelization period was observed. A supportive study made on granuloma tissue to estimate the levels of superoxide-dismutase, catalase, glutathione, vitamin c and lipid peroxidation are recorded and a significant increase in the level of these antioxidant enzymes and decrease in the levels of lipid peroxidation was observed. Enhanced wound healing activity may be due to free radical scavenging action of the NAC and the enhanced level of antioxidant enzymes in granuloma tissue. Better collagenation may be because of improved antioxidant studies.

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Repositioning drugs for traumatic brain injury - N-acetyl cysteine and Phenserine

Repositioning drugs for traumatic brain injury - N-acetyl cysteine and Phenserine

Traumatic brain injury (TBI) is one of the most common causes of morbidity and mortality of both young adults of less than 45 years of age and the elderly, and contributes to about 30% of all injury deaths in the United States of America. Whereas there has been a significant improvement in our understanding of the mechanism that underpin the primary and secondary stages of damage associated with a TBI incident, to date however, this knowledge has not translated into the development of effective new pharmacological TBI treatment strategies. Prior experimental and clinical studies of drugs working via a single mechanism only may have failed to address the full range of pathologies that lead to the neuronal loss and cognitive impairment evident in TBI and other disorders. The present review focuses on two drugs with the potential to benefit multiple pathways considered important in TBI. Notably, both agents have already been developed into human studies for other conditions, and thus have the potential to be rapidly repositioned as TBI therapies. The first is N-acetyl cysteine (NAC) that is currently used in over the counter medications for its anti-inflammatory properties. The second is ( − )-phenserine (( − )-Phen) that was originally developed as an experimental Alzheimer ’ s disease (AD) drug. We briefly review background information about TBI and subsequently review literature suggesting that NAC and ( − )-Phen may be useful therapeutic approaches for TBI, for which there are no currently approved drugs.

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Studies on the Chemopreventive Potential of N-acetyl cysteine/ zinc oxide nanocomposite combined with High ascorbate  on 7,12-dimethylbenz(a)anthracene Induced Mammary Carcinogenesis in Rats

Studies on the Chemopreventive Potential of N-acetyl cysteine/ zinc oxide nanocomposite combined with High ascorbate on 7,12-dimethylbenz(a)anthracene Induced Mammary Carcinogenesis in Rats

1. DMBA play a role in the development of mammary gland carcinoma and this effect may be mediated by inhibition of Casepase-3 and Casepase-9 resulting in inhibition of apoptosis and cause carcinogenesis. 2. N-acetyl cysteine /Zinc oxide Nano composite and high pH ascorbate attenuates carcinogenic effects of DMBA on rat mammary glands and reverses DMBA- induced suppression of caspases -3 and -9 activity. Collectively, these observations suggested that novel synthetic Nano composite may potentially presents new hope for the development of breast cancer prevention, which should attract further scientific & pharmaceutical interest.

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N acetyl cysteine and mushroom Agaricus sylvaticus supplementation decreased parasitaemia and pulmonary oxidative stress in a mice model of malaria

N acetyl cysteine and mushroom Agaricus sylvaticus supplementation decreased parasitaemia and pulmonary oxidative stress in a mice model of malaria

Background: Malaria infection can cause high oxidative stress, which could lead to the development of severe forms of malaria, such as pulmonary malaria. In recent years, the role of reactive oxygen species in the pathogenesis of the disease has been discussed, as well as the potential benefit of antioxidants supplementation. The aim of this study was to investigate the effects of N-acetyl cysteine (NAC) or mushroom Agaricus sylvaticus supplementation on the pulmonary oxidative changes in an experimental model of malaria caused by Plasmodium berghei strain ANKA. Methods: Swiss male mice were infected with P. berghei and treated with NAC or AS. Samples of lung tissue and whole blood were collected after one, three, five, seven or ten days of infection for the assessment of thiobarbituric acid reactive substances (TBARS), trolox equivalent antioxidant capacity (TEAC), nitrites and nitrates (NN) and to assess the degree of parasitaemia.

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The protective effect of N-acetyl cysteine against carbon tetrachloride toxicity in rats

The protective effect of N-acetyl cysteine against carbon tetrachloride toxicity in rats

Khan & Ahmed, 2009 and Abdel Moneim, 2016). More- over, the free radicals of CCl4 bind with the unsaturated fatty acid of sperm plasma membrane forming alkoxy and peroxy radicals; as a result, lipid peroxides are produced, which are extremely reactive leading to alteration in sperm concentration, modification of the hormonal levels, and in- duction of necrosis (Ogeturk et al., 2005). Free radicals also induce decrease in GSH content, oxidative DNA dam- ages, DNA adducts, DNA fragmentation, chromosomal ab- errations and genetic mutations (Jia, Han, & Chen, 2002; Khan, Rizvi, Khan, Khan, & Shaheen, 2009 and Ahmed et al., 2014), germ cells necrosis, and degeneration in the testicular tubules (Guo, Lu, & Hsu, 2005 and Horn et al., 2006). On the other hand, N-acetyl cysteine (NAC), a po- tent antioxidant, has been utilized clinically for the treat- ment of many diseases (Rodrigues, Eiora, & Schaff, 2004; Akgun et al., 2005; Atkuri, Mantovani, Herzenberg, & Herzenberg, 2007; Sadowska, Manuel, & de Backer, 2007; Baker et al., 2009 and Samuni, Goldstein, Dean, & Berk, 2013). It is a small membrane permeable molecule that can rapidly permeate the intracellular sections. This anti- oxidant has a diversity of applications, mostly because of the reduced thiol moiety existing in its structure, which can scavenge reactive oxygen species (ROS) directly, and indirectly, NAC protects the liver by being hydrolyzed into cysteine; this, in turn, plays a significant role in the pro- duction of glutathione (Pereira-Filho et al., 2008) and enhancement of glutathione-S-transferase activity leading to the intracellular defense against oxidative stress and promotes detoxification (Aremu, Madejczyk, & Ballatori, 2008). Previous studies revealed the protective effects of NAC against CCl4-induced hepatotoxicity (Ritter, Reinke, Andrades, et al., 2004; Maksimchik, Lapshina, Sudnikovich, Zabrodskaya, & Zavodnik, 2008, Sahin and Alatas 2010), nephrotoxicity (Hanly et al., 2013 and Ustyol et al., 2017), and genotoxicity (Gurbuz, Ozkul, & Burgaz, 2009). There- fore, the present study was designated to investigate whether NAC has a protective effect on the toxicity of CCl4 by its antioxidant actions through biochemical, histopatho- logical, and genetic investigations.

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The effect of combined N acetyl cysteine and vitamin C supplementation on blood biomarkers during single bout of exhaustive exercise in wistar rats

The effect of combined N acetyl cysteine and vitamin C supplementation on blood biomarkers during single bout of exhaustive exercise in wistar rats

Exhausting physical activity can cause harmful effects on the human, due to release of free radicals. This research is focused on effect of combined N-acetyl cysteine (NAC) and vitamin C (VC) supplementation on biomarkers of blood total antioxidant capacity (TAC), malondialdehyde (MDA) and C- reactive protein (CRP) during the exhaustive exercise in Wistar rats. This study was carried out on 32 female Wistar rats, which divided into 4 groups. In First group was given the effervescent tablets (NAC 600 mg, dissolved in water) four hours before the experiment by gavages. Second group received VC tablets (500 mg) and for third, a combination of VC and NAC (VICNAC), and fourth, was taken as the control group. Three stages of Blood samples were taken 1hour before starting, immediately after the exhaustive exercise, and after one hour at rest, respectively. After separating the serum samples; they were immediately stored at -80 ◦ C until analysis. The MDA, CRP and TAC concentrations were respectively measured using spectrophotometric and ELISA methods. A Significant reduction was observed in the concentration of MDA immediately after the exhaustive exercise in NAC group, in compared with the control (P ≤0.05); as well as CRP level in VICNAC group (P ≤0.05). There was no change in the TAC blood concentration during the study except in the NAC group one hour after exercise, which was significantly decreased in compared with the control groups (P≤0.05). In Conclusion, The results demonstrated that oral administration of NAC at least four hours before an exhaustive exercise can significantly decrease the harmful effects of oxidative stress in rats.

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Simultaneous Determination of N Acetyl Cysteine and Taurine by HPTLC Method in Active Pharmaceutical Ingredient and Pharmaceutical Dosage Form

Simultaneous Determination of N Acetyl Cysteine and Taurine by HPTLC Method in Active Pharmaceutical Ingredient and Pharmaceutical Dosage Form

As per the literature survey there have been no reports on High Performance Thin Layer Chromatographic method for quantitative analysis of N-Acetyl cyste- ine and Taurine in both active pharmaceutical ingredients (APIs) and marketed tablet formulation. Hence the present study was intended for the development of a method for the simultaneous estimation of N-Acetyl cysteine and Taurine in active pharmaceutical ingredient and tablet dosage form and to validate as per ICH guidelines.

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Effect of N-Acetyl Cysteine on Liver Function in General Anesthesia with Isoflurane

Effect of N-Acetyl Cysteine on Liver Function in General Anesthesia with Isoflurane

Oxidative stress is the results of imbalance between free radicals of oxygen and internal anti-oxidant systems. N-acetyl cysteine is the most common external anti-oxidant which is used to deal with oxidative damages caused to tissue. The anti-oxidant influence of N-acetyl cysteine is due to its direct effects or the secondary effects caused by higher rates of Glutathione production. Its direct effect is reaction with hydroxyl radicals and deactivation of them. N- acetyl cysteine also prevents wasting glutathione and increases the levels of glutathione in liver. In an animal sample of acute kidney damage, glutathione could prevent Ischemic damages 20 . In

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N-acetyl cysteine-loaded graphene oxide-collagen hybrid membrane for scarless wound healing

N-acetyl cysteine-loaded graphene oxide-collagen hybrid membrane for scarless wound healing

N-acetyl cysteine (NAC) is a compound approved by the U.S. Food and Drug Administration for clinical use as a mucolytic which has thiol and carboxyl groups [33, 34]. NAC may have a broader therapeutic potential, particularly in the setting of antioxidants [35]. Recently, Zayed et al observed that NAC could accelerate amputation stump healing by increased neovascularization casting new light on its use in wound healing [36]. Besides, NAC can reduce the ROS level of the injured area, thus protecting the functional cells from the damage caused by excessive ROS [37]. Theoretically, the -COOH of NAC makes it possible to form an amide linkage with collagen and GO and enable sustained release.

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A comparative study of hepatoprotective effect of curcumin with  n acetyl cysteine and their simultaneous administration in  acetaminophen induced hepatotoxicity

A comparative study of hepatoprotective effect of curcumin with n acetyl cysteine and their simultaneous administration in acetaminophen induced hepatotoxicity

Ever since 1970, acetaminophen overdose has been alarmingly countries and has been an important cause for hospital admission in developed countries like in United Kingdom, United States, Europe and Australia. (Sheen et al., The most important outcome of acetaminophen overdose be fatal. Current standard of treatment is N acetyl cysteine (NAC), as it supplies sulfhydryl groups for regeneration of reduced glutathione. (Sheen et al., Liver transplantation as an option is very limited, owing high costs. Data of the prevalence of acetaminophen overdose is available for the developed nations. However, in the developing nations and Asian populations the data has been scarce. In a study by

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N ACETYL CYSTEINE ALLEVIATES PHENYTOIN INDUCED BEHAVIORAL ABNORMALITIES IN RATS

N ACETYL CYSTEINE ALLEVIATES PHENYTOIN INDUCED BEHAVIORAL ABNORMALITIES IN RATS

Our work is a preliminary and pioneering study to assess the ameliorative effect of NAC against phenytoin induced behavioral abnormalities. Phenytoin and its metabolites are reported to induce oxidative stress in brain regions via free radical generation leading to behavioral abnormalities. Thus it is worthwhile to explore the protective effect of NAC against phenytoin induced behavioral abnormalities. The influence of NAC against phenytoin impaired memory; exploratory behavior, spontaneous motor activity and locomotor activity were studied along with estimation of regional brain lipid peroxidation and acetyl cholinesterase (ACh E) activity. Our hypothesis proposes that antioxidant property of NAC offers protection against phenytoin induced behavioral abnormalities. Antioxidant supplementation is suggested to render an excellent antiepileptic therapy devoid of toxicity which may improve the quality of life in patients under phenytoin treatment.

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Aflatoxicosis in rabbits with particular reference to its control by n  acetyl cysteine and probiotic

Aflatoxicosis in rabbits with particular reference to its control by n acetyl cysteine and probiotic

AFB1-mediated toxicity was also found to be related to its pro- oxidant potential. This is because reactive oxygen species (ROS) including superoxide anion (O-), hydrogen peroxide (H2O2) and hydroxyl radical (-OH) that are generated during the metabolic processing of AFB1by liver enzymes, Preston and Wiliams (2005). Also, ROS at higher concentration are important mediators of damage to cell structures, including lipids, membranes, proteins and nucleic acids oxidative stress (Poli et al., 2004). AFB1-DNA adduction is believed to be the source of point mutations that initiate AFB1-induced hepato- carcinogenesis (Bailey et al., 1996). The harmful effects of ROS are balanced by the antioxidant action of non-enzymatic antioxidants in addition to antioxidant enzymes (Hallowell, 1996). Numerous physical, chemical and biological methods had been proposed to detoxify or inactivate aflatoxins in contaminated feedstuffs. Supplementation with antioxidants, through an increased consumption in the diet either has become extremely popular as a means to improve animal and human health or increase their physical performance. The addition of chemical compounds to animal feed as N-acetyl-L-cysteine (NAC)a thiol containing anti-oxidant had been used to mitigate various conditions of oxidative stress. In addition, it reduces liver injury caused by paracetamol over dosage in human, attenuates liver injury, and prevents liver and plasma GSH depletion in mice and rabbits (Flanagan and Mereditht, 1991 and Kelly, 1998). On the other hand, the biological methods by using microorganisms and their metabolites in feed and/or water to eliminate aflatoxins, can be a highly promising approach owing to its specific, efficient and environmentally friendly detoxification Some microbes, including fungal and bacterial isolates (FAO, 2001 and Nabawy et al., 2014). Therefore, the current study was undertaken to demonstrate the prevalence of fungi and aflatoxins in rabbit’s environment and

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Dendrimer-mediated delivery of N-acetyl cysteine to microglia in a mouse model of Rett syndrome

Dendrimer-mediated delivery of N-acetyl cysteine to microglia in a mouse model of Rett syndrome

We have previously shown that in the presence of neu- roinflammation, generation-4 hydroxyl-terminated poly(- amidoamine) (G4-OH PAMAM) dendrimers (~ 4 nm) cross the blood-brain barrier (BBB) and accumulate se- lectively in activated microglia and astrocytes in the brain of newborn rabbits with cerebral palsy (CP), but not in age-matched healthy controls [32]. These same dendrimers accumulate in activated glia in a canine model of hypothermic circulatory arrest-induced brain injury [33] and in a mouse model of ischemia-induced neonatal white matter injury [34]. The goal of this study was to determine whether methyl-CpG-binding protein 2 mouse gene ( Mecp2 )-null glia respond differently to an inflammatory stimulus when compared to wild-type (WT) glia, and if dendrimer-conjugated N -acetyl cyst- eine (D-NAC) is effective in attenuating these responses in the KO and WT glia. We also evaluated whether D- NAC bypasses the Xc − transporter to deliver NAC and cysteine intracellularly which would improve intracellu- lar glutathione levels without increasing extracellular glutamate. As a translational application of this concept, we also explored the potential of this glial cell-directed therapy using D-NAC administered after symptom on- set, for improvement in neurological outcomes in a clin- ically relevant mouse model of RTT.

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Effects of N-Acetyl Cysteine on Oxidative Stress Biomarkers in End-stage Renal Disease

Effects of N-Acetyl Cysteine on Oxidative Stress Biomarkers in End-stage Renal Disease

Background and Objective: Imbalance between the oxidants and antioxidants in biologic systems is called oxidative stress which is associated with wide range of diseases and malfunctions. Renal physiology, high blood flow and reabsorption mechanisms make kidneys susceptible organs to oxidative stress, especially in End-Stage Renal Disease (ESRD) patients; because of their decreased antioxidant capacity along with increased oxidant species. N-Acetyl cysteine (NAC) is a known synthetic antioxidant. Our aim of study was to investigate helpful antioxidant effects of NAC on oxidative stress biomarkers in ESRD patients.

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Amyloid β peptide-induced inhibition of endothelial nitric oxide production involves oxidative stress-mediated constitutive eNOS/HSP90 interaction and disruption of agonist-mediated Akt activation

Amyloid β peptide-induced inhibition of endothelial nitric oxide production involves oxidative stress-mediated constitutive eNOS/HSP90 interaction and disruption of agonist-mediated Akt activation

eNOS phosphorylation at Set1179 (Figure 9). These ob- served alterations appear to be the result of oxidative damage because the concomitant treatment of the cells with the antioxidant N-acetyl cysteine reverts Aβ effects restoring a normal pattern of eNOS phosphorylation at serine 1179 and interaction with HSP-90 (Figures 4 and 8). Our data demonstrated for the first time an inverse effect of Aβ on HSP90/eNOS interaction and HSP90/Akt inter- action. We confirmed that upon stimulation with VEGF, Akt phosphorylates eNOS in an HSP90-dependent man- ner; synergistically increasing eNOS activity (Figures 1, 6, and 7). Once Aβ is introduced to these conditions, there is a diminished interaction between HSP90 and Akt, sug- gesting that the chaperone remains bound to eNOS in a manner that facilitates its inability to sufficiently bind Akt to signal its phosphorylation at Ser473 (Figures 9 and 10). Although the partial loss of this interaction could occur

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Thiol suppression of human immunodeficiency virus type 1 replication in primary cord blood monocyte derived macrophages in vitro

Thiol suppression of human immunodeficiency virus type 1 replication in primary cord blood monocyte derived macrophages in vitro

We investigated the effects of glutathione (GSH), the major naturally occurring thiol, and a pharmacologic thiol precursor of GSH, N-acetyl cysteine (NAC), on the expression of human immunodeficiency type 1 (HIV-1) in primary cord blood and adult donor monocyte- derived macrophages (MDM). HIV-1 infection of cord blood and adult MDM was

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CYSTEINE –MASTER ANTIOXIDANT

CYSTEINE –MASTER ANTIOXIDANT

N-acetyl cysteine (NAC) is modified form of cystine a non essential amino acid wherein an acetyl group is attached to the nitrogen atom that can be manufactured in the liver which helps the body make the antioxidants enzyme glutathione. . This compound is sometimes considered as a dietary supplement. NAC is often used as a cough medicine as it breaks up the disulfide bonds in the mucus and thus liquefies it, easier to cough up. Several studies have found that it is beneficial to people with chronic bronchitis and there is preliminary evidence to suggest that it may help prevent colon cancer. It is believed by some that NAC may help to promote hair growth and prevents hair loss. It is also used as nutrient in baby milk formula and dietary suppliments. Scientists in Finland believe that cysteine containing chewing gum could become a new way of preventing upper digestive tract cancers.

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N-Acetyl L-Cysteine does not protect mouse ears from the effects of noise*

N-Acetyl L-Cysteine does not protect mouse ears from the effects of noise*

Background: Noise-induced hearing loss (NIHL) is one of the most common occupational injuries in the United States. It would be extremely valuable if a safe, inexpensive compound could be identified which protects worker hearing from noise. In a series of experiments, Kopke has shown that the compound N-acetyl-L-cysteine (L-NAC) can protect the hearing of chinchillas from the effects of a single exposure to noise. L-NAC is used in clinical medicine and is very safe. Although L-NAC was reported to be promising, it has not been successful in other studies (Kramer et al., 2006; Hamernik et al., 2008). The present study was undertaken to determine if L-NAC could protect C57BL/6J (B6) mice from the permanent effects of noise.

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In vivo transfer of nitric oxide between a plasma protein bound reservoir and low molecular weight thiols

In vivo transfer of nitric oxide between a plasma protein bound reservoir and low molecular weight thiols

corresponding LMW S-nitrosothiol. The transfer of NO from albumin to L-cysteine was directly measured in rabbit plasma using a novel technique that couples high performance liquid chromatography to electrochemical detection. These data demonstrate that NO exchange between plasma protein thiol-bound NO and available LMW thiol pools (transnitrosation) occurs in vivo.

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Impaired nuclear factor erythroid 2-related factor 2 expression increases apoptosis of airway epithelial cells in patients with chronic obstructive pulmonary disease due to cigarette smoking

Impaired nuclear factor erythroid 2-related factor 2 expression increases apoptosis of airway epithelial cells in patients with chronic obstructive pulmonary disease due to cigarette smoking

all cell types and tissues, and is most abundant in tissues where detoxification reactions occur routinely, including the lungs. However, Nrf2 is also inducible and triggered by oxidative stress, injury, and inflammation. Cigarette smoke contains a substantial ROS, and exposure to cigarette smoke is known to induce transient Nrf2 ex- pression in human airway cells. Upon stimulation, cyto- solic Nrf2 reaches the nucleus and binds to ARE in the upstream promoter region of antioxidant genes and ini- tiates transcription [4]. Among these, the glutathione cysteine ligase catalytic subunit (GCLC) and glutathione cysteine ligase modifier subunit (GCLM) are important for antioxidant defense. Nrf2 is required for the consti- tutive and inducible expression of GCLC and GCLM, which are required for glutathione (GSH) synthesis [14]. Impaired Nrf2 expression in COPD patients might fail to evoke an appropriate antioxidant response and allow excessive apoptosis resulting in lung tissue destruction and emphysema. A previous cohort study showed that certain polymorphisms of the Nrf2 gene correlated with accelerated limitations in airflow of smokers [15, 16]. Subjects with impaired Nrf2 might be related to COPD.

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