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. 2024 Jan 19;12(1):87. doi: 10.3390/toxics12010087

Table 1.

Assays to predict MIE and KEs for cardiotoxicity.

ASSAYS to Increase of Oxidative Stress ASSAYS to Increase in Mitochondrial Dysfunction ASSAYS to Inhibition of Mitochondrial Complexes
APR HepG2 P-H2AX 24 h dn APR HepG2 MitoMass 24 h dn CCTE Simmons MITO basal resp rate OCR dn
APR HepG2 P-H2AX 24 h up APR HepG2 MitoMass 24 h up CCTE Simmons MITO basal resp rate OCR up
APR HepG2 P-H2AX 72 h dn APR HepG2 MitoMass 72 h dn CCTE Simmons MITO inhib resp rate OCR dn
APR HepG2 P-H2AX 72 h up APR HepG2 MitoMass 72 h up CCTE Simmons MITO inhib resp rate OCR up
APR HepG2 StressKinase 24 h dn APR HepG2 MitoMembPot 24 h dn CCTE Simmons MITO max resp rate OCR dn
APR HepG2 StressKinase 24 h up APR HepG2 MitoMembPot 24 h up CCTE Simmons MITO max resp rate OCR up
APR HepG2 StressKinase 72 h dn APR HepG2 MitoMembPot 72 h dn
APR HepG2 MitoMembPot 72 h up
ATG XTT Cytotoxicity up
TOX21 MMP ratio down
TOX21 MMP ratio up
TOX21 MMP rhodamine