N-acetyl-cysteine prevents toxic oxidative effects induced by IFN-α in human neurons
Open accessAbstract
Currently IFN-α is widely used for effective treatment of viral infections and several malignancies. However, IFN-α can cause neuropsychiatric disturbances and mental impairments, including fatigue, insomnia, depression, irritability and cognitive deficits. Molecular and cellular mechanisms leading to such side-effects are still poorly understood. Neurons seem to be an important target in mediating cellular effects induced by exposure to this cytokine, but so far little is known about IFN-α-induced effects on these cells. We have investigated the ability of IFN-α (2-100 ng/ml) to induce damage and toxicity to the human neuroblastoma SH-SY5Y cell line, commonly used for studying such phenomena, and the mechanisms underlying these effects. After 24 h treatment, IFN-α increased mitochondrial activity, whereas cell density was reduced in a dose- and time-dependent manner. This effect did not depend on reduced cell proliferation, but rather the activation of apoptosis, as revealed by an increased Bax:Bcl-2 mRNA ratio after 72-h IFN-α exposure. At this time-point, IFN-α also reduced the expression of the brain-derived neurotrophic factor gene, and induced an increase in reactive oxygen species (ROS). A co-treatment with N-acetyl-cysteine (NAC; 5 mm), a potent antioxidant and mitochondrial modulator, was able to counteract all of these IFN-α-induced effects. These findings demonstrated that IFN-α induces neurotoxicity and apoptosis that is, in part, very likely due to mitochondrial damages and production of ROS. We suggest that NAC, already tested for the treatment of psychiatric disorders, may be useful to prevent IFN-α-induced central side-effects in a safe and effective way.
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The detrimental effects of these inflammatory stimuli can be reversed by antidepressant treatments including inhibitors of kynurenine pathways, antioxidants and mitochondrial modulators, and omega-3 polyunsaturated fatty acids.
“We also showed that the detrimental effects of these inflammatory stimuli can be reversed by antidepressant treatments as diverse as inhibitors of the kynurenine pathways, antioxidants and mitochondrial modulators, and omega-3 polyunsaturated fatty acids”
From Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation (2017) · cites this paper as Alboni et al., 2013
The effect of IL-1 and interferon-alpha on neurogenesis and survival is mediated by increased production of neurotoxic tryptophan metabolites and increased oxidative stress.
“an effect that is mediated by an increased production of neurotoxic tryptophan metabolites as well as an increased oxidative stress”
From Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation (2017) · cites this paper as Alboni et al., 2013
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- Authors
- Alboni, S., Gibellini, L., Montanari, C., Benatti, C., Benatti, S., Tascedda, F., Brunello, N., Cossarizza, A., & Pariante, C. M.
- Affiliations
- University of Modena and Reggio Emilia (IT)
- King's College London (GB)
- ORCID
- Venue
- International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-09-01
- Volume
- 16
- Issue
- 8
- Pages
- 1849-1865
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- OpenAlex
- W2141096613
- Cited by
- 35
- References
- 70
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 5 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 2 · 2014: 4 · 2013: 1
- FWCI
- 1.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- IRIS UNIMORE (University of Modena and Reggio Emilia) (submittedVersion, cc-by)
- Research Portal (King's College London) (submittedVersion)
- Funders
- European College of Neuropsychopharmacology
- Società Italiana di Farmacologia
- Medical Research Council (MR/J002739/1)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- interferon-alpha, N-acetylcysteine, neurotoxicity, apoptosis, reactive oxygen species, mitochondrial damage, oxidative stress, Bax/Bcl-2 ratio, brain-derived neurotrophic factor, SH-SY5Y cells, antioxidant defense
- MeSH terms
- Acetylcysteine, Analysis of Variance, Bromodeoxyuridine, Cell Differentiation, Dose-Response Relationship, Drug, Flow Cytometry, Gene Expression Regulation, Humans, Neuroblastoma, RNA, Messenger, Time Factors, Tretinoin, Tumor Necrosis Factor-alpha, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Brain-Derived Neurotrophic Factor, Proto-Oncogene Proteins c-bcl-2, In Situ Nick-End Labeling, Cell Line, Tumor, Cell Proliferation, bcl-2-Associated X Protein
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