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However, it remains mechanistically unclear about how to maintain mTORC1 activity during mammary glands development. Here we showed that mammary glands suffered from aggravated oxidative stress as pregnancy advanced and was accompanied by an increase in H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> levels, while the consumption for methionine and <jats:italic>S<\/jats:italic>\u2010adenosylmethionine (SAM) rather than <jats:italic>S<\/jats:italic>\u2010adenosylhomocysteine (SAH) were promoted <jats:italic>in vivo<\/jats:italic>. Likewise, H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> promoted SAM synthesis and reduced SAM utilization for methylation depending on H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> levels and treatment time <jats:italic>in vitro<\/jats:italic>. H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> inhibited phosphorylation of S6 kinase Thr 389 (p\u2010S6K1 (T389)), 4E\u2010BP1 Thr 37\/46 and ULK1 Ser 757, the downstream of mTORC1, in mammary epithelial cells. However, methionine and SAM were shown to activate mTORC1 under H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2010exposed condition. Moreover, this effect was not disabled by SGI\u20101027 which inhibits SAM transmethylation. In conclusion, methionine appeared to protect mammary cells against oxidative stress through producing SAM to maintain mTORC1 signaling activity.<\/jats:p>","DOI":"10.1155\/2021\/5550196","type":"journal-article","created":{"date-parts":[[2021,7,20]],"date-time":"2021-07-20T22:05:15Z","timestamp":1626818715000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Methionine Protects Mammary Cells against Oxidative Stress through Producing S\u2010Adenosylmethionine to Maintain mTORC1 Signaling 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