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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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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

been used as drug carriers, cosmetics, and fillings in medical materials [4]. Nano-Zinc oxide (nZnO) is a new product with particle diameter between 1-100 nm [5]. Recently, nZnO has been considered as an important factor in the area of animal science [6]. It appears that nano materials hold excessive potential to pass some of the barriers to efficient targeting of cells and molecules in many diseases [7,8]. Supplementation of cells with antioxidants can help alleviate this oxidative stress. For instance, N-Acetyl Cysteine (NAC) is a cell permeant glutathione precursor, which can be used to replenish the cellular stores of the molecule that donates an electron to reactive oxygen, thereby neutralizing its reactivity [9].
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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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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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Combined Effect of N-Acetyl Cysteine and Clarithromycin on Bleomycin Induced Pulmonary Fibrosis

Combined Effect of N-Acetyl Cysteine and Clarithromycin on Bleomycin Induced Pulmonary Fibrosis

Combined therapy with clarithromycin (CLTR) and N–acetyl cysteine (NAC) may be useful in diseases with impaired oxidant-antioxidant balance, fibroblast proliferation, and collagen deposition such as pulmonary fibrosis. Activated inflammatory cells which accumulate in the lower airways may release increased amounts of reactive oxygen species (ROS) when accompanied with a deficiency in glutathione, the major component of the lung antioxidant defense system, leading to lung injury and fibrosis. The aim of this study was to examine the combined effect of CLTR, and NNAC on bleomycin-induced lung fibrosis in rats. Bleomycin was administered by single intra tracheal instillation to Wistar rats to induce lung fibrosis. Rats under study were orally administered with NAC (3 mmol/Kg), and CLTR (20 mg/Kg) from day 4 to 21, after a single intra tracheal instillation of bleomycin (2.5 U/Kg) or saline on day 1. Combined treatment with CLTR and NAC significantly decreased the augmented collagen deposition in bleomycin exposed rats (P< 0.05). Hydroxyproline content was 1.711±0.94 mg/g/tissue, and 1.055±1.83 mg/g/tissue in bleomycin-treated (positive control), and CLTR + NAC treated rats, respectively. CLTR and NAC combined therapy resulted in a significant increase (P< 0.05) in GSH (22%), significant decrease (P< 0.05) in MDA (14%), and significant decrease (P< 0.05) in total protein levels (39%) when compared to positive control rats. The histological assessment using a semi quantitative score showed less collagen deposition, and inflammatory cells in CLTR + NAC treated rats compared to those receiving bleomycin alone. Additionally, hematological and clinical chemistry parameters of blood did not revealed any signs of toxicity of combined treatment. These results indicate that combined treatment with NAC and CLTR improves the pulmonary antioxidant protection, collagen deposition, and thus might be useful in reducing lung damage produced by bleomycin.
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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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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

[14] Holdiness, M.R., Morgan, L.R., Gillen, L.E. and Harrison, E.F. (1986) High Perfor- mance Liquid Chromatographic Determination of N-Acetyl Cysteine in Human Se- rum Following Acetaminophen Over Dosage. Journal of Chromatography B , 382, 99-106. [15] Orlovic, D., Radulovic, D. and Vujic, Z. (2004) Determination of S-Carboxy Me- thyl-L-Cysteine, Methylparaben and their Degradation Products in Syrup Prepara- tions. Chromatographia , 60, 329-333. https://doi.org/10.1365/s10337-004-0371-0 [16] Hannested, U. and Sorbo, B. (1979) Determination of 3-Mercaptolactate, Mercap-
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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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The Antioxidant Role of Glutathione and N-Acetyl-Cysteine Supplements and Exercise-Induced Oxidative Stress

The Antioxidant Role of Glutathione and N-Acetyl-Cysteine Supplements and Exercise-Induced Oxidative Stress

transduction of gene expression. Many pathological states, such as cancer, Parkinson’s disease, and Alzheimer’s disease have been shown to be related to the redox state of cells. In an attempt to minimize the onset of oxidative stress, supplementation with various known antioxidants has been suggested. Glutathione and N-acetyl-cysteine (NAC) are antioxidants which are quite popular for their ability to minimize oxidative stress and the downstream negative effects thought to be associated with oxidative stress. Glutathione is largely known to minimize the lipid peroxidation of cellular membranes and other such targets that is known to occur with oxidative stress. N-acetyl-cysteine is a by-product of glutathione and is popular due to its cysteine residues and the role it has on glutathione maintenance and metabolism. The process of oxidative stress is a complicated, inter-twined series of events which quite possibly is related to many other cellular processes. Exercise enthusiasts and researchers have become interested in recent years to identify any means to help minimize the detrimental effects of oxidative stress that are commonly associated with intense and
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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-loaded graphene oxide-collagen hybrid membrane for scarless wound healing

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

Wound dressings composed of natural polymers, such as type I collagen, possess good biocompatibility, water holding capacity, air permeability, and degradability, and can be used in wound repair. However, due to the persistent oxidative stress in the wound area, the migration and proliferation of fibroblasts might be suppressed, leading to poor healing. Thus, collagen-containing scaffolds are not suitable for accelerated wound healing. Antioxidant N-acetyl cysteine (NAC) is known to reduce the reactive oxygen species (ROS) and has been widely used in the clinic. Theoretically, the carboxyl group of NAC allows loading of graphene oxide (GO) for sustained release and may also enhance the mechanical properties of the collagen scaffold, making it a better wound-dressing material. Herein, we demonstrated an innovative approach for a potential skin-regenerating hybrid membrane using GO incorporated with collagen I and NAC (N-Col-GO) capable of continuously releasing antioxidant NAC.
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Comparative evaluation of reversal of shear bond strength on bleached enamel using antioxidants – sodium ascorbate, salicylic acid & N-acetyl cysteine: An in vitro study

Comparative evaluation of reversal of shear bond strength on bleached enamel using antioxidants – sodium ascorbate, salicylic acid & N-acetyl cysteine: An in vitro study

Hence the purpose of this study was to evaluate the effect of 3 antioxidant agents [Sodium ascorbate, Salicylic acid, N-acetyl cysteine] on reversal of the shear bond strengths of compos[r]

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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

The occurrence of toxicity in various organs was examined since volatile anesthetics have been used clinically. Among the complications the liver toxicity is very important. Due to the effects of N-Acetyl Cysteine (NAC), we decided to conduct a study to assess liver function in patients undergoing anesthesia with isoflurane and received NAC to evaluate its effects on the liver complications of these anesthetics. In this double- blind clinical trial, 68 patients between 20 to 60 years old candidate for elective surgery with a time duration between 1 to 3 hours (except surgeries on the liver and biliary tract) were enrolled and randomly divided into two groups, N-acetylcysteine and control. To check liver function, the levels of AST, ALT, LDH, PT, aPTT and INR was measured in the preoperative, 1 hour and 24 hours after surgery. The results of the study showed that there was significant difference between the levels of ALT (p=0.0001), AST (p=0.0001), and LDH (p=0.0001) between two groups. Heart rate was also significantly different between groups (p=0.0001) but the difference in systolic (p=0.096) and diastolic (p=0.174) blood pressure was not significant. N-acetyl cysteine is an antioxidant medication and its effects on excreting organs such as the kidneys and liver is frequently evaluated. In this study, n-acetyl cysteine could significantly reduce liver enzyme levels after administration of isoflurane, compared to the control group.
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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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N ACETYL CYSTEINE ALLEVIATES PHENYTOIN INDUCED BEHAVIORAL ABNORMALITIES IN RATS

N ACETYL CYSTEINE ALLEVIATES PHENYTOIN INDUCED BEHAVIORAL ABNORMALITIES IN RATS

ABSTRACT: NAC being an antioxidant combats oxidative stress induced by phenytoin, thereby hypothesized to reduce phenytoin induced behavioral abnormalities. The influence of N acetyl cysteine (NAC) supplementation on phenytoin induced behavioral abnormalities was investigated. Male Wistar rats were divided into 5 groups and each group received vehicle (0.2% CMC), Phenytoin (20mg/Kg), Phenytoin co administered with three graded doses of NAC (50, 100, 200 mg/kg) in 0.2% CMC for 45 days. Motor coordination, exploratory behavior, memory and spontaneous motor activity were evaluated by Rota rod, Hole board, Elevated plus maze and Actophotometer respectively. On day 45, regional brain lipid peroxidation, acetylcholinesterase (ACh E) activity and histopathological studies were performed after euthanasia. In addition, pharmacokinetic and pharmacodynamic drug interactions between phenytoin and NAC were also studied. Long term administration of phenytoin induced behavioral abnormalities, elevated regional brain malondialdehyde (MDA) and ACh E activity, also revealed congestion in addition to damaged cells in brain regions. NAC significantly prevented phenytoin induced behavioral abnormalities, oxidative stress and reversed the histopathological abnormalities. There were no significant differences in the serum levels of phenytoin and the degree of protection offered by phenytoin in NAC supplemented groups revealing that there were no pharmacokinetic and pharmacodynamic interactions between phenytoin and NAC. This study demonstrates that NAC is effective in preventing phenytoin induced behavioral abnormalities and oxidative stress in rats without altering the serum phenytoin levels and its therapeutic effect. This suggests the potential of adjuvant NAC therapy in alleviating behavioral disturbances induced by chronic phenytoin therapy.
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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

To determine whether L -cysteine, NAC, and D-NAC were dependent on system Xc − for intracellular trans- port and increasing glutathione levels, LPS-activated BV2 cells were treated with L -cysteine, NAC, or D-NAC (all at 100 μg/mL of cysteine or NAC basis) in the pres- ence or absence of sulfasalazine, a potent Xc − inhibitor (50 μM that is not toxic to BV2 cells; the schematic is shown in Fig. 5 top panel). Activation of the BV2 cells with LPS led to a 50% reduction in baseline levels of GSH ( p < 0.0001; Fig. 5b) and ~ 2.5-fold higher levels of extra- cellular glutamate (Fig. 5a). Although treatment with L - cysteine and NAC led to an increase in intracellular GSH levels, treatment with D-NAC at the same dose (on a NAC basis) was significantly better [ F (2,21) = 54.75, p < 0.0001; Fig. 5a]. Treatment with NAC and L -cysteine was associated with an increase in extracellular glutamate [ F (4,72) = 11.28, p < 0.001] that was not seen with D-NAC treatment. Extracellular glutamate levels were lower in D-NAC and D-NAC + sulfasalazine-treated cells than in NAC and L -cysteine ( p < 0.05 and p < 0.01, respectively; Fig. 5b). This increase in glutamate with NAC and L - cysteine treatment was attenuated when sulfasalazine was applied for Xc − inhibition, indicating that Xc − is involved in cysteine and NAC transport into the cell. Inhibition of Xc − with sulfasalazine also prevented the increase in intracellular GSH seen with L -cysteine treat- ment, but this was not seen with NAC. This indicates that although Xc − may be the primary mechanism of transport of cysteine and NAC intracellularly, it is possible that other mechanisms of NAC transport may become involved when Xc − is inhibited, which may help increase cellular glutathione levels. However, the re- sponse to D-NAC treatment (a significant increase in glutathione without an increase in extracellular glutam- ate) was seen irrespective of sulfasalazine treatment, indicating that D-NAC bypasses this antiporter.
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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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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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Effect of Hypobaric Hypoxia on Cognitive Functions and Potential Therapeutic Agents

Effect of Hypobaric Hypoxia on Cognitive Functions and Potential Therapeutic Agents

impairments may include neuronal damage, oxidative stress and neurotransmitter alterations. Jayalakshmi et al. 2007 (28), reported that N-acetyl cysteine (NAC) administration during HBH exposure ameliorated the hypoxia-induced impairments in spatial working memory function. In addition, NAC supplementation decreased oxidative stress, increased the antioxidant status, and reduced free radical production during HBH. Other study suggests that acetyl-L-carnitine supplementation improved the spatial working memory deficits of rats chronically exposed to HBH (24). Additionally, Barhwal et al. 2009 (23) suggested that L-type calcium channels and glutamate receptors play an important role in learning and memory functions during HBH. They reported that isradipine, an L-type calcium channel blocker, may serve as a useful therapeutic agent to improve spatial memory during HBH. Further more, bacosides ameliorated the memory impairment induced by exposure to HBH (25). Also, bacosides upregulated NCAM, enhanced cytochrome c oxidase activity, and improved memory during HBH. Hota et al. 2008 (29), concluded that ceftriaxone ameliorated HBH- induced cognitive impairment. Alternatively, Baitharu et al. 2012 (30,31), suggested that corticosterone plays a role in learning and memory functions during HBH. They reported that the administration of the corticosterone synthesis inhibitor metyrapone and Withania somnifera root extract improved cognitive functions during HBH. Besides, Muthuraju et al. 2009, 2010, and 2011 reported that physostigmine and galantamine ameliorated the increase in the level of acetylcholinesterase during and after HBH exposure and enhanced cholinergic system function. This facilitation of the cholinergic system may help to improve learning and memory during HBH. Prasad et al. 2013, reported that Quercetin reverses cognitive impairment by reducing the level of oxidative stress. Furthermore, Vishal et al. 2012 (36), found that an enriched environment prevented HBH-induced memory impairment. Based on these studies, the aforementioned therapeutic agents may ameliorate HBH-induced cognitive impairment.
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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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