Table 1.

Ability of Mitochondrial Targeted Antioxidants to Modulate Lytic Programmed Cell Death in the Context of Acute Inflammation in Different Experimental Animal Models

Antioxidant	Dose	Effect on programmed cell death	Experimental model	Function/mechanism	References
MitoTEMPO	20 mg/kg (i.p.)	Necroptosis prevention	Murine model of APAP hepatotoxicity	Avoid mitochondrial peroxynitrite formation	Du et al. (2019)
MitoTEMPO	25 mg/kg (i.p.)	Necroptosis prevention	Murine model of acute pancreatitis (cerulein) in sulfiredoxin KO mice	Avoid Prx3 hyperoxidation	Rius-Pérez et al. (2022)
MitoQ	10 mg/kg (2 doses)	No change	Murine model of acute pancreatitis (cerulein)	Avoid mitochondrial ROS formation	Huang et al. (2015)
MitoQ	25 mg/kg (2 doses)	Tendency to increase necrosis	Murine model of acute pancreatitis (cerulein)	Avoid mitochondrial ROS formation	Huang et al. (2015)
XJB-5-131	0.1 μM	Ferroptosis prevention	HT-1080 cells	Avoid mitochondrial lipid peroxidation	Krainz et al. (2016)
MitoQ	1 μM	Ferroptosis prevention	HT22 cells	Avoid mitochondrial ROS formation	Jelinek et al. (2018)
MitoQ	1 μM	Ferroptosis prevention	MEF cells	Avoid mitochondrial ROS formation	Jelinek et al. (2018)
MitoTEMPO	5 mg/kg (i.p.)	Ferroptosis prevention	Murine model of DOX-induced cardiomyopathy	Avoid mitochondrial lipid peroxidation	Fang et al. (2019)
SS-31	50 or 100 μg/mL	Pyroptosis prevention	Nucleus pulposus cells	Avoid mitochondrial ROS formation	Peng et al. (2021)
MitoTEMPO	20 mg/kg (i.p.)	Pyroptosis prevention	Murine model of LPS-induced Sepsis	Avoid mitochondrial ROS formation	Wang et al. (2022)

DOX, doxorubicin; LPS, lipopolysaccharide; Prx3, peroxiredoxin 3; ROS, reactive oxygen species.