Table 1.

Mitochondrial damage during sepsis

Species	Inducer	Tissue/cell	Time/stage	Mitochondrial assessments	Refs.
Human	N.A	PBMCs	With shock	Oxygen consumption reduced; ATP synthase activity declined	[15]
Human	N.A	PBMCs	Early stages without shock or MOF	CI, CIII, and CIV activity decreased; ΔΨm reduced; Oxygen consumption reduced; Circulating free mtDNA in plasma increased	[16]
Human	N.A	Platelet	Severe sepsis or septic shock	Mitochondrial NADH, CI, CI & III, and CIV, succinate dehydrogenase (SDH) activity decreased	[17]
Human	N.A	Leg and serratus anterior muscle	With MOF and requiring mechanical ventilation	Leg muscle: CI activity unchanged; CIV activity and ATP reduced; morphology unchanged Serratus anterior muscle: CI activity decreased; CIV activity, ATP, and morphology unchanged The observed changes probably because of reduced mitochondrial mass	[28]
Human	N.A	Vastus lateralis muscle	With MOF	Structure swollen or damaged; Respiratory protein subunits and transcripts reduced	[19]
Human	N.A	Heart	Post-mortem	Mitochondrial cristae impaired	[20]
Mouse	LPS	Heart	24 h	Mitochondrial number and volume reduced; Mitochondrial displayed internal vesicles, disrupted structure, and loss of cristae; expression of OXPHOS genes decreased	[29]
Mouse	LPS	Kidney	18 h	Mitochondrial swollen and cristae reduced; Cytochrome c oxidase protein level and activity decreased; Mitochondrial gene expression was suppressed	[30]
Mouse	LPS	Liver	0–48 h	mtDNA levels/integrity, complex I activity, and ATP level reduced; mtROS increased	[31]
Mouse	LPS	Leg muscle	28 days	Mitochondrial respiration reduced; CV activity was reduced; Mitochondrial fission increased;	[32]
Mouse	CLP	Brain	24 h	Oxidative phosphorylation uncoupled; ΔΨm dissipated; CIV activity reduced; CI-III activity unchanged	[33]
Mouse	CLP	Heart	12 h	mtDNA copy number reduced; mitochondrial respiration reduced; ATP level declined; mitochondrial biogenesis marker PGC1β reduced; mitochondrial Ca2+ uptake capacity declined	[34]
Mouse	CLP	Kidney	6–36 h	ROS increased; CI, CII & CIII activity and ATP decreased; CIV activity unchanged	[35]
Rat	LPS	Heart	0–24 h	Mitochondria displayed structural abnormalities; CI, II, and IV activities reduced; ATP synthesis decreased	[36]
Rat	LPS	Liver	2 h	Mitochondrial oxygen consumption reduced despite the total oxygen consumption unchanged; mitochondria became swollen and pale, with indistinct cristae and disrupted membranes; ATP/ADP ratio unchanged	[37]
Rat	S. pneumoniae	Heart	24 h	ROS increased; mtDNA damaged; mitochondrial membrane disrupted; CI, II-III, IV and V activity reduced	[38]
Cat	LPS	Liver	4 h	Respiratory activity was impaired; mitochondrial ultrastructural injured (swollen and membrane disruption)	[39]
Baboon	E. coli	Heart	72 h or after death	CI, and II activities reduced; CIII was less affected	[25]

MOF multi-organ failure. CI, II, III, IV, V: mitochondrial respiratory complex I, II, III, IV, V. ΔΨm: mitochondrial membrane potential