Protective effects of N-acetyl-cysteine in mitochondria bioenergetics, oxidative stress, dynamics and S-glutathionylation alterations in acute kidney damage induced by folic acid

2019 ◽  
Vol 130 ◽  
pp. 379-396 ◽  
Author(s):  
Omar Emiliano Aparicio-Trejo ◽  
Laura María Reyes-Fermín ◽  
Alfredo Briones-Herrera ◽  
Edilia Tapia ◽  
Juan Carlos León-Contreras ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Kidney Damage ◽  
Protective Effects ◽  
Acetyl Cysteine

Effect of alpha-ketoglutarate and N-acetyl cysteine on cyanide-induced oxidative stress mediated cell death in PC12 cells

2010 ◽  
Vol 26 (5) ◽  
pp. 297-308 ◽  
Author(s):  
RM Satpute ◽  
J. Hariharakrishnan ◽  
R. Bhattacharya
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Critical Role ◽  
Total Antioxidant Status ◽  
Protective Effects ◽  
Simultaneous Treatment ◽  
Acetyl Cysteine

Cyanide is a mitochondrial poison, which is ubiquitously present in the environment. Cyanide-induced oxidative stress is known to play a key role in mediating the neurotoxicity and cell death in rat pheochromocytoma (PC12) cells. PC12 cells are widely used as a model for neurotoxicity assays in vitro. In the present study, we investigated the protective effects of alpha-ketoglutarate (A-KG), a potential cyanide antidote, and N-acetyl cysteine (NAC), an antioxidant against toxicity of cyanide in PC12 cells. Cells were treated with various concentrations (0.625—1.25 mM) of potassium cyanide (KCN) for 4 hours, in the presence or absence of simultaneous treatment of A-KG (0.5 mM) and NAC (0.25 mM). Cyanide caused marked decrease in the levels of cellular antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR). Lipid peroxidation indicated by elevated levels of malondialdehyde (MDA) was found to be accompanied by decreased levels of reduced glutathione (GSH) and total antioxidant status (TAS) of the cells. Cyanide-treated cells showed notable increase in caspase-3 activity and induction of apoptotic type of cell death after 24 hours. A-KG and NAC alone were very effective in restoring the levels of GSH and TAS, but together they significantly resolved the effects of cyanide on antioxidant enzymes, MDA levels, and caspase-3 activity. The present study reveals that combination of A-KG and NAC has critical role in abbrogating the oxidative stress-mediated toxicity of cyanide in PC12 cells. The results suggest potential role of A-KG and NAC in cyanide antagonism.

scholarly journals Folic Acid Attenuated Learning and Memory Impairment via Inhibition of Oxidative Damage and Acetylcholinesterase Activity in Hypothyroid Rats

2021 ◽  
Author(s):  
Sabiheh Amirahmadi ◽  
Mahmoud Hosseini ◽  
Somaieh Ahmadabady ◽  
Mahsa Akbarain ◽  
Kataneh Abrari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Oxidative Damage ◽  
Learning And Memory ◽  
Cognitive Performance ◽  
Ache Activity ◽  
Acetylcholinesterase Activity ◽  
Protective Effects ◽  
Thiol Content ◽  
Oxidative Stress Indicators

Abstract Hypothyroidism has been associated with cognitive decline. Considering the role that has been suggested for folic acid (FA) in cognitive performance, the present study was designed to investigate the effects of FA against hypothyroidism-induced cognitive impairment, oxidative damage and acetylcholinesterase (AChE) activity alterations in propylthiouracil (PTU)-induced hypothyroid rats. In this study, PTU (0.05% in drinking water) and FA (5, 10, and 15 mg/kg, oral gavage) were administered to the rats for a period of 7 weeks. Then, behavioral performance was tested using Morris water maze (MWM) and passive avoidance (PA) tasks. Finally, oxidative stress indicators and AChE activity were assayed in the brain tissues. The impairing effect of hypothyroidism on cognitive performance was markedly alleviated by FA especially at the higher doses. In the MWM test, FA reduced escape latency and travelled distance, compared to the non-treated hypothyroid group. In the PA test, the latency to enter the dark chamber was significantly enhanced by FA as compared to the non-treated hypothyroid group (p < 0.05-p < 0.001). Besides, FA attenuated AChE activity and malondialdehyde level but increased superoxidase dismutase enzyme activity and total thiol content (p < 0.05-p < 0.001). In conclusion, FA could improve learning and memory ability in hypothyroid rats. The observed protective effects may be mediated through regulation of oxidative stress and AChE activity.

Protective effects of melatonin and N-acetyl cysteine against oxidative stress induced by microcystin-LR on cardiac muscle tissue

Toxicon ◽  
2019 ◽  
Vol 169 ◽  
pp. 38-44 ◽  
Author(s):  
Leila Ait Abderrahim ◽  
Khaled Taïbi ◽  
Nawel Ait Abderrahim ◽  
Anas M. Alomery ◽  
Fatiha Abdellah ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Muscle ◽  
Muscle Tissue ◽  
Protective Effects ◽  
Acetyl Cysteine

scholarly journals The Protective Effects of Enalapril Maleate and Folic Acid Tablets against Contrast-Induced Nephropathy in Diabetic Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jiantong Hou ◽  
Gaoliang Yan ◽  
Bo Liu ◽  
Boqian Zhu ◽  
Yong Qiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Endothelial Dysfunction ◽  
Diabetic Rats ◽  
Tunel Staining ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Contrast Induced Nephropathy ◽  
Enalapril Maleate ◽  
Renal Vasoconstriction

Background. Renal vasoconstriction, oxidative stress, endothelial dysfunction, and apoptosis are the major causes of contrast-induced nephropathy (CIN). The aim of this study was to evaluate the protective effects of enalapril maleate and folic acid tablets on CIN in diabetic rats.Methods. Thirty-two Sprague-Dawley rats were divided into four groups: CIN (C), CIN + enalapril maleate (CE), CIN + folic acid (CF), and CIN + enalapril maleate and folic acid tablets (CEF). CE, CF, and CEF rats were treated orally with enalapril maleate, folic acid, or enalapril maleate and folic acid tablets, respectively, for 5 days. CIN was induced in all groups followed by analyzed biochemical parameters, oxidative stress markers, endothelial dysfunction parameters, renal histopathology, and TUNEL staining.Results. Serum creatinine, blood urea nitrogen, and malondialdehyde levels were lower in the CEF group than in the C group. Homocysteine, superoxide dismutase, glutathione peroxidase, and nitric oxide levels were higher in the CEF group than in the C group. Histopathology scores and percentage of apoptotic kidney cells in the CEF group were significantly decreased compared with those in the C group.Conclusions. These results suggest that enalapril maleate and folic acid tablets have a protective effect against CIN in diabetic rats.

Protective Effects of α-Tocopherol and N-Acetyl-Cysteine on Diazinon-Induced Oxidative Stress and Acetylcholinesterase Inhibition in Rats

2007 ◽  
Vol 17 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Shahin Shadnia ◽  
Mojgan Dasgar ◽  
Sepideh Taghikhani ◽  
Azadeh Mohammadirad ◽  
Reza Khorasani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acetylcholinesterase Inhibition ◽  
Protective Effects ◽  
Acetyl Cysteine

scholarly journals Drug-Induced Liver Injury: Clinical Evidence of N-Acetyl Cysteine Protective Effects

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yonela Ntamo ◽  
Khanyisani Ziqubu ◽  
Nireshni Chellan ◽  
Bongani B. Nkambule ◽  
Tawanda M. Nyambuya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Clinical Evidence ◽  
Antioxidant Properties ◽  
Pathological Feature ◽  
Protective Effects ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Acetyl Cysteine

Oxidative stress is a key pathological feature implicated in both acute and chronic liver diseases, including drug-induced liver injury (DILI). The latter describes hepatic injury arising as a direct toxic effect of administered drugs or their metabolites. Although still underreported, DILI remains a significant cause of liver failure, especially in developed nations. Currently, it is understood that mitochondrial-generated oxidative stress and abnormalities in phase I/II metabolism, leading to glutathione (GSH) suppression, drive the onset of DILI. N-Acetyl cysteine (NAC) has attracted a lot of interest as a therapeutic agent against DILI because of its strong antioxidant properties, especially in relation to enhancing endogenous GSH content to counteract oxidative stress. Thus, in addition to updating information on the pathophysiological mechanisms implicated in oxidative-induced hepatic injury, the current review critically discusses clinical evidence on the protective effects of NAC against DILI, including the reduction of patient mortality. Besides injury caused by paracetamol, NAC can also improve liver function in relation to other forms of liver injury such as those induced by excessive alcohol intake. The implicated therapeutic mechanisms of NAC extend from enhancing hepatic GSH levels to reducing biomarkers of paracetamol toxicity such as keratin-18 and circulating caspase-cleaved cytokeratin-18. However, there is still lack of evidence confirming the benefits of using NAC in combination with other therapies in patients with DILI.

scholarly journals Folic Acid Protects Melanocytes from Oxidative Stress via Activation of Nrf2 and Inhibition of HMGB1

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Pengran Du ◽  
Shaolong Zhang ◽  
Shuli Li ◽  
Yuqi Yang ◽  
Pan Kang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Therapeutic Potential ◽  
Antioxidant Properties ◽  
Vital Role ◽  
Related Factor ◽  
Protective Effects ◽  
Abnormal Growth ◽  
Oxidative Damages ◽  
Human Melanocytes

Vitiligo is a cutaneous depigmentation disease due to loss of epidermal melanocytes. Accumulating evidence has indicated that oxidative stress plays a vital role in vitiligo via directly destructing melanocytes and triggering inflammatory response that ultimately undermines melanocytes. Folic acid (FA), an oxidized form of folate with high bioavailability, exhibits potent antioxidant properties and shows therapeutic potential in multiple oxidative stress-related diseases. However, whether FA safeguards melanocytes from oxidative damages remains unknown. In this study, we first found that FA relieved melanocytes from H2O2-induced abnormal growth and apoptosis. Furthermore, FA enhanced the activity of antioxidative enzymes and remarkably reduced intracellular ROS levels in melanocytes. Subsequently, FA effectively activated nuclear factor E2-related factor 2 (Nrf2) pathway, and Nrf2 knockdown blocked the protective effects of FA on H2O2-treated melanocytes. Additionally, FA inhibited the production of proinflammatory HMGB1 in melanocytes under oxidative stress. Taken together, our findings support the protective effects of FA on human melanocytes against oxidative injury via the activation of Nrf2 and the inhibition of HMGB1, thus indicating FA as a potential therapeutic agent for the treatment of vitiligo.

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