N-acetyl-L-cysteine reduces arsenite-induced cytotoxicity through chelation in U937 monocytes and macrophages

Ghani, Sidra; Khan, Noureen; Koriyama, Chihaya; Akiba, Suminori; Yamamoto, Megumi

doi:10.3892/mmr.2014.2612

Cited by 8 publications

(4 citation statements)

References 32 publications

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“…In this study, the addition of NAC suppressed the MeHg‐stimulated cytokine expressions. NAC is known to suppress toxicity of MeHg and other heavy metals such as arsenic (Aremu et al ., ; Ghani et al ., ; Samuni et al ., ). We have reported that NAC suppressed the MeHg‐induced cytokine production through both inhibition of reactive oxygen species as well as extracellular chelation of MeHg in U‐87 MG cells (Muniroh et al ., ).…”

Section: Discussionmentioning

confidence: 98%

Activation of interleukin‐6 and ‐8 expressions by methylmercury in human U937 macrophages involves RelA and p50

Yamamoto

Khan

Muniroh

et al. 2016

J of Applied Toxicology

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The accumulation of macrophages has been observed around lesions of the brain in patients with Minamata disease. In this condition, mercury has been detected histochemically in macrophages throughout the brain. However, the role of macrophages in the neurotoxicity of methylmercury (MeHg) and the molecular mechanisms of their response to MeHg exposure remain to be elucidated. Here, we investigated how MeHg affects the expression of proinflammatory cytokines such as interleukin (IL)-6 and IL-8 in cultured human U937 macrophages. Compared with controls, IL-6 and IL-8 mRNA expression was maximally induced in U937 macrophages after treatment with 10 μM MeHg for 6 h. The protein secretion of IL-6 and IL-8 was significantly stimulated by MeHg in U937 macrophages. Results from luciferase reporter assay indicated functional activation of nuclear factor kappa B and the involvement of subunit RelA and p50 in MeHg-induced IL-6 and IL-8 activation, which was confirmed by siRNA knockdown experiments. MeHg exposure at 4 μM also significantly induced IL-8 expression in U-87 MG cells at mRNA and protein level, indicating that IL-8 induction might be a general mode of action of MeHg treatment among different cell types. These results indicate a possible involvement of an early inflammatory response, including IL-6 and IL-8 expression in the pathogenesis of MeHg. N-acetyl-l-cysteine suppressed MeHg-induced activation of IL-6 and IL-8 mRNA expression in U937 macrophages, indicating the effectiveness of N-acetyl-l-cysteine as a therapeutic drug in MeHg-induced inflammation. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Discussionmentioning

confidence: 98%

Activation of interleukin‐6 and ‐8 expressions by methylmercury in human U937 macrophages involves RelA and p50

Yamamoto

Khan

Muniroh

et al. 2016

J of Applied Toxicology

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“…It reduces ROS level by raising intracellular glutathione (GSH) concentrations and/or playing directly as a free radical scavenger [19], and inhibits transcription factor activation in upstream signaling, which is important for inflammatory and oxidative stress responses [20,31,37]. Furthermore, it also acts as a chelating agent for heavy metals and accelerates urinary excretion of MeHg in mice [5,17].…”

Section: Introductionmentioning

confidence: 99%

Suppression of methylmercury-induced IL-6 and MCP-1 expressions by N-acetylcysteine in U-87MG human astrocytoma cells

et al. 2015

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“…(Jiao et al, 2016; Pedre et al, 2021). NAC showed cytotoxicity preventive effects on U937 monocytes and human kidney epithelial cells (HK-2 cell line) (Zhang et al, 2011; Ghani et al, 2014). Similarly, we showed that treating mouse fibroblast cells (L929) and macrophage cells (J774A.1) with NAC up to a concentration of 100mg/mL had no cytotoxicity even after 30 minutes of exposure.…”

Section: Discussionmentioning

confidence: 99%

Successfully treating biofilms of extensively drug resistant Klebsiella pneumoniae isolates from hospital patients with N-Acetyl Cysteine

Chauhan

Bhowmik

Rohit

2022

Preprint

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Klebsiella pneumoniae is one of the leading causes of community and nosocomial infections. Reduced treatment options against extensively drug resistant (XDR) - K. pneumoniae, is a serious concern in hospital settings, and hence, WHO has categorized it as a critical priority pathogen. Biofilm forming ability is a common virulence mechanism amongst K. pneumoniae that is associated with antibiotic tolerance up to 1000X MIC and hence, are difficult to treat. N-acetyl cysteine (NAC) is an FDA approved mucolytic drug used to treat acetaminophen-associated toxicity and obstructive pulmonary diseases. In this study, we assessed antibacterial and antibiofilm activity of NAC against clinical isolates of XDR K. pneumoniae, obtained from Madras Medical Mission Hospital, India. To assess the biofilm eradication ability of NAC, we grew biofilms in 96 well plates and treated the mature biofilms with different concentrations of NAC. We observed that the biofilms of only 3 isolates of XDR K. pneumoniae could be eradicated at a concentration as low as 20mg/ml. Although increasing the concentration of NAC to 80mg/mL could significantly reduce the biofilms of all the isolates up to 4-5 Log, NAC at a concentration of 100 mg/mL successfully eradicated the mature biofilms of all the isolates of XDR K. pneumoniae. This in vitro study demonstrates the potential of NAC as an efficient agent against the biofilms of clinical isolates of XDR-K. pneumoniae and thus provides a promising alternative to antibiotics.

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N-acetyl-L-cysteine reduces arsenite-induced cytotoxicity through chelation in U937 monocytes and macrophages

Cited by 8 publications

References 32 publications

Activation of interleukin‐6 and ‐8 expressions by methylmercury in human U937 macrophages involves RelA and p50

Activation of interleukin‐6 and ‐8 expressions by methylmercury in human U937 macrophages involves RelA and p50

Suppression of methylmercury-induced IL-6 and MCP-1 expressions by N-acetylcysteine in U-87MG human astrocytoma cells

Successfully treating biofilms of extensively drug resistant Klebsiella pneumoniae isolates from hospital patients with N-Acetyl Cysteine

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