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Therefore, early intervention in replenishing mGSH stores by supplying GSH precursor such as N -acetylcysteine (NAC) or targeting upstream mechanisms involved in mitochondrial dysfunction and ROS generation, such as the sustained activation of c-Jun N-terminal kinases (JNK), can result in the protection of APAP-mediated hepatotoxicity

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Supplementary material The Supplementary Material for this article can be found online at: Supplementary Video 1 BCG intercellular localization inside B16-F10 tumor cells

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10.1038/s41598-020-64173-3 Sci