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. Author manuscript; available in PMC: 2020 Dec 1.
Published in final edited form as: J Biol Inorg Chem. 2019 Nov 21;24(8):1305–1316. doi: 10.1007/s00775-019-01740-8

Figure 4. Mechanisms of iAs-induced cell death in neuronal cells.

Figure 4

iAs neurotoxicity has been related to the activation of different cell death pathways. (a) Exposure to iAs and its methylated metabolites induces caspase-dependent apoptosis, involving the activation of the mitogen-activated protein kinase (MAPK) pathways, specifically c-Jun N-terminal kinase (JNK), p38 and extracellular-signal-regulated kinase (ERK) which are associated with the intrinsic mitochondrial apoptotic pathway. iAs also triggers intracellular calcium (Ca2+) increase that mediates apoptosis. (b) iAs-induced cell death is regulated by autophagy activation through the activation of the AMP-dependent protein kinase (AMPK) and inhibition of the mechanistic (or mammalian) target of rapamycin (mTOR).