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

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.

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 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.

Protective Effects of Chungkookjang Extract on High Glucose Induced Oxidative Stress in LLC-PK1Cells

2008 ◽  
Vol 13 (2) ◽  
pp. 84-89 ◽  
Author(s):  
Na-Ri Yi ◽  
Kyoung-Chun Seo ◽  
Ji-Myung Choi ◽  
Eun-Ju Cho ◽  
Young-Ok Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Protective Effects

Protective effects of andrographolide derivative AL-1 on high glucose-induced oxidative stress in RIN-m cells

2016 ◽  
Vol 22 (4) ◽  
pp. 499-505 ◽  
Author(s):  
Hui Yan ◽  
Yongmei Li ◽  
Yali Yang ◽  
Zaijun Zhang ◽  
Gaoxiao Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
M Cells ◽  
Protective Effects

Effects of Montmorillonite on Growth Performance, Serum Biochemistry and Oxidative Stress of Red-Crowned Crane (Grus japonensis) Fed Mycotoxin-Contaminated Feed

2020 ◽  
Vol 21 (8) ◽  
pp. 626-632 ◽  
Author(s):  
Dawei Liu ◽  
Qinghua Wu ◽  
Hongyi Liu ◽  
Changhu Lu ◽  
Chao Gu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Performance ◽  
Feed Intake ◽  
Animal Feed ◽  
Bird Species ◽  
Serum Biochemistry ◽  
Protective Effects ◽  
Regular Diet ◽  
Grus Japonensis ◽  
And Oxidative Stress

Background: The red-crowned crane (Grus japonensis) is one of the most vulnerable bird species in the world. Mycotoxins are toxic secondary metabolites produced by fungi and considered naturally unavoidable contaminants in animal feed. Our recent survey indicated that the mycotoxins had the potential to contaminate redcrowned crane’s regular diets in China. Objective: This experiment was conducted to investigate the protective effects of mycotoxin binder montmorillonite (Mont) on growth performance, serum biochemistry and oxidative stress parameters of the red-crowned crane. Methods: 16 red-crowned cranes were divided into four groups and fed one of the following diets; a selected diet, regular diet, or the selected diet or regular diet with 0.5% montmorillonite added to the diets. The cranes' parameters of performance, hematology, serum biochemistry and serum oxidative stress were measured. Results: Consuming regular diets decreased the average daily feed intake (ADFI), levels of haemoglobin (Hb), platelet count (PLT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), but increased the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine kinase (CK) and lactate dehydrogenase (LDH). The supplementation of 0.5% Mont provided protection for the red-crowned crane in terms of feed intake, serum biochemistry and oxidative stress. Moreover, Mont supplementation had no adverse effect on the health of red-crowned crane. Conclusions: Taken together, these findings suggested that the addition of dietary Mont is effective in improving the health of red-crowned crane.

scholarly journals Protective Effects of GYY4137 on Renal Ischaemia/Reperfusion Injury through Nrf2-Mediated Antioxidant Defence

2021 ◽  
pp. 1-9
Author(s):  
Hongmei Zhao ◽  
Yun Qiu ◽  
Yichen Wu ◽  
Hong Sun ◽  
Sumin Gao
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Nuclear Translocation ◽  
Organ Damage ◽  
Related Factor ◽  
Protective Effects ◽  
Ischaemia Reperfusion Injury ◽  
Renal Ischaemia ◽  
Ischaemia Reperfusion ◽  
Renal Histology

<b><i>Introduction/Aims:</i></b> Hydrogen sulfide (H<sub>2</sub>S) is considered to be the third most important endogenous gasotransmitter in organisms. GYY4137 is a long-acting donor for H<sub>2</sub>S, a gas transmitter that has been shown to prevent multi-organ damage in animal studies. We previously reported the effect of GYY4137 on cardiac ischaemia reperfusion injury (IRI) in diabetic mice. However, the role and mechanism of GYY4137 in renal IRI are poorly understood. The aims of this study were to determine whether GYY4137 can effectively alleviate the injury induced by renal ischaemia reperfusion and to explore its possible mechanism. <b><i>Methods:</i></b> Mice received right nephrectomy and clipping of the left renal pedicle for 45 min. GYY4137 was administered by intraperitoneal injection for 2 consecutive days before the operation. The model of hypoxia/reoxygenation injury was established in HK-2 cells, which were pre-treated with or without GYY4137. Renal histology, function, apoptosis, and oxidative stress were measured. Western blot was used to measure the target ­protein after renal IRI. <b><i>Results:</i></b> The results indicated that GYY4137 had a clear protective effect on renal IRI as reflected by the attenuation of renal dysfunction, renal tubule injury, and apoptosis. Moreover, GYY4137 remarkably reduced renal IRI-induced oxidative stress. GYY4137 significantly elevated the nuclear translocation of nuclear factor-erythroid-2-related factor 2 (Nrf2) and the expression of antioxidant enzymes regulated by Nrf2, including SOD, HO-1, and NQO-1. <b><i>Conclusions:</i></b> GYY4137 alleviates ischaemia reperfusion-induced renal injury through activating the antioxidant effect mediated by Nrf2 signalling.

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