Table 1: List of compounds investigated in TAMH and their general effects.

AgentDrug classPathways affectedReference(s)

APAPAnalgesic(i) ATP depletion
(ii) GSH depletion
(iii) Induces Jnk activation
(iv) Upregulation of ETC protein components
(v) Activation of p53 signaling
[31, 39, 40, 44]

TFECN/A; fluorocarbon metabolite(i) Nrf2 induction and increased expression of ARE response genes
(ii) Induction of ER-stress response genes
(iii) Cell death is Bax-mediated (antagonized by Bcl-xl overexpression)
(iv) Upregulation of Hsps
[12, 55, 81]

FlutamideAntiandrogen(i) Upregulation of Nrf2 response genes
(ii) Downregulation of fatty acid β-oxidation genes Mitochondrial dysfunction (ATP depletion, complex I inhibition)

PD035901MEK inhibitor(i) Inhibits ERK activation
(ii) Inhibited cell growth

LapatinibTyrosine kinase inhibitor(i) Cyp3a induction (dexamethasone) increased cell death[67]

FlupirtineAnalgesic(i) Toxicity not directly linked to oxidative processes[72]