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Studies indicate that neural stem cell (NSC) self\u2010renewal is susceptible to oxidative stress caused by xenobiotics. However, the impact of antioxidants on NSC self\u2010renewal and the potential mechanisms remain elusive. In this study, primary murine neural progenitor cells (mNPCs) from the subventricular zone were used as a research model. In addition, paraquat (PQ) was used to elicit oxidative stress and <jats:italic>N<\/jats:italic>\u2010acetylcysteine (NAC) was used as a powerful antioxidant. mNPCs were treated with 80\u00a0\u03bc<jats:sc>m<\/jats:sc> PQ for 24\u00a0hours with or without 4\u00a0hours of NAC pretreatment. Our results showed that PQ treatment increased intracellular reactive oxygen species production, decreased cell viability and DNA synthesis, and promoted cell apoptosis. Meanwhile, pretreatment with NAC alleviated PQ\u2010induced cytotoxicity in mNPCs. To elucidate the mechanisms further, we found that NAC pretreatment prevented PQ\u2010induced reactive oxygen species production, mitochondrial fragmentation and autophagy in mNPCs. NAC\u2010pretreated cells showed increased anti\u2010apoptotic protein Bcl\u20102 and decreased pro\u2010apoptotic protein Bax expression. Similarly, NAC pretreatment increased p\u2010mTOR and decreased LC3B\u2010II protein expression. Moreover, NAC decreased mitophagy related mRNA <jats:italic>Pink1<\/jats:italic> and <jats:italic>Parkin<\/jats:italic> expression. Taken together, our results suggested that the antioxidant NAC treatment significantly attenuated PQ\u2010induced mNPC self\u2010renewal disruption through decreasing autophagy and salvaging mitochondrial morphology. These findings revealed a potential mechanism for neurological treatment relating to antioxidant and suggested potentially relevant implications for PQ\u2010related neurodegenerative disorders. Thus, our study also provided insight into therapeutic strategies for the neurotoxic effects of oxidative stress\u2010associated toxicants.<\/jats:p>","DOI":"10.1002\/jat.3839","type":"journal-article","created":{"date-parts":[[2019,8,1]],"date-time":"2019-08-01T05:37:01Z","timestamp":1564637821000},"page":"1557-1567","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["<i>N<\/i>\u2010acetylcysteine alleviated paraquat\u2010induced mitochondrial fragmentation and autophagy in primary murine neural progenitor cells"],"prefix":"10.1002","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0492-9111","authenticated-orcid":false,"given":"Guiya","family":"Xiong","sequence":"first","affiliation":[{"name":"School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education Fudan University  Shanghai China"},{"name":"The Department of Science and Research The Second Affiliated Hospital 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