ArticlePloS one2019
N-acetyl cysteine attenuates oxidative stress and glutathione-dependent redox imbalance caused by high glucose/high palmitic acid treatment in pancreatic Rin-5F cells.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Antiglycation approach in selected autoimmune diseases: Where do we stand?Redox biology · 2026Review
- Plasma exosome-derived miRNA-887-5p alleviates high glucose- and lipid-induced endothelial cell dysfunction.Nutrition & diabetes · 2026Article
- Morphological and Biochemical Insights Into the Renoprotective Effects of Combined N-Acetylcysteine and Glycine Treatment in Experimental Diabetic Nephropathy.Pharmacology research & perspectives · 2026Article
- Redefining the role of the thiol-based agentRSC medicinal chemistry · 2026Review
- Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026Review
- High palmitate induces ferroptosis in RIN-m5f cells via miR-3584-5p-mediated suppression of AQP7.Scientific reports · 2026Article
- Effects of N-acetyl-L-cysteine on sperm quality during chilled storage of Maguan hornless goat semen.PloS one · 2026Article
- Effect of Fatty Acids on Glucose Metabolism and Type 2 Diabetes.Nutrition reviews · 2025Review
- New horizon of the combined BCG vaccine with probiotic and liraglutide in augmenting beta cell survivalHeliyon · 2024Article
- L-NAC and L-NAC methyl ester prevent and overcome physical dependence to fentanyl in male rats.Scientific reports · 2024Article
- Article
- Azadirachtin Attenuates Carcinogen Benzo(a) Pyrene-Induced DNA Damage, Cell Cycle Arrest, Apoptosis, Inflammatory, Metabolic, and Oxidative Stress in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Spore Oil-Functionalized Selenium Nanoparticles Protect Pancreatic Beta Cells from Palmitic Acid-Induced Apoptosis via Inhibition of Oxidative Stress-Mediated Apoptotic Pathways.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Pancreas-Liver-Adipose Axis: Target of Environmental Cadmium Exposure Linked to Metabolic Diseases.Toxics · 2023Review
- L-NAC reverses of the adverse effects of fentanyl infusion on ventilation and blood-gas chemistry.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Article
- Small-molecule discovery in the pancreatic beta cell.Current opinion in chemical biology · 2022Review
- Circular RNA PIP5K1A act as microRNA-552-3p sponge to regulates inflammation, oxidative damage in glucolipotoxicity-induced pancreatic INS-1 β-cells via Janus kinase 1.Bioengineered · 2022Article
- Effect of Photo-Mediated Ultrasound Therapy on Nitric Oxide and Prostacyclin from Endothelial Cells.Applied sciences (Basel, Switzerland) · 2022Article
- Alterations in Inflammatory Cytokines and Redox Homeostasis in LPS-Induced Pancreatic Beta-Cell Toxicity and Mitochondrial Stress: Protection by Azadirachtin.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Elevated levels of glucose and fatty acids are the main characteristics of diabetes, obesity and other metabolic disorders, associated with increased oxidative stress, mitochondrial dysfunction and inflammation. Once the primary pathogenesis of diabetes is established, which is potentially linked to both genetic and environmental factors, hyperglycemia and hyperlipidemia exert further destructive and/or toxic effects on β-cells. The concept of glucolipotoxicity has arisen from the combination of deleterious effects of chronic elevation of glucose and fatty acid levels on pancreatic β- cell function and/or survival. Though numerous studies have been conducted in this field, the exact molecular mechanisms and causative factors still need to be established. The aim of the present work was to elucidate the molecular mechanisms of oxidative stress, and inflammatory/antioxidant responses in the presence of high concentrations of glucose/fatty acids in a cell-culture system using an insulin-secreting pancreatic β-cell line (Rin-5F) and to study the effects of the antioxidant, N-acetyl cysteine (NAC) on β-cell toxicity. In our study, we investigated the molecular mechanism of cytotoxicity in the presence of high glucose (up to 25 mM) and high palmitic acid (up to 0.3 mM) on Rin-5F cells. Our results suggest that the cellular and molecular mechanisms underlying β-cell toxicity are mediated by increased oxidative stress, imbalance of redox homeostasis, glutathione (GSH) metabolism and alterations in inflammatory responses. Pre-treatment with NAC attenuated oxidative stress and alterations in GSH metabolism associated with β-cells cytotoxicity.
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