Table 1.

Summary of potential mechanisms involved in impaired OPC differentiation linked to oxidative stress

Mechanism of interest	Description	Effect of oxidative stress	Direct evidence?
nDNA and mtDNA damage	Base modifications (8-oxoG)	Increase	+
	SSB and DSB	Increase	+
DNA repair	Excision repair (NER, BER)	Higher need	+
	Recombinational repair (DSBR)	Higher need	+
	Competing demand: differentiation vs. DNA repair	Increase	±
Epigenetics	HAT and HDAC balance	Altered	+
	Methylation pattern changes	Altered	±
	MiRNA activity and biogenesis	Altered	±
Mitochondria	ETC function	Decrease	±
	ROS generation	Increase	+
Cell signalling	ROS-sensitive signalling in relation to cell growth, metabolism, differentiation and antioxidant defence (e.g. AMPK, MAPK, PGC-1α, Nrf2, mTOR)	Altered	±

 +  = direct evidence linking oxidative stress to the mechanism of interest in OPCs, ±  = suggested link but no direct evidence linking oxidative stress to the mechanisms in OPCs yet. 8-oxoG 8-oxo-7,8-dihydroguanine, BER base excision repair, DSB double-strand breaks, DSBR double-strand break repair, ETC electron transport chain, HAT histone acetyltransferases, HDAC histone deacetylases, NER nucleotide excision repair, OPC oligodendrocyte precursor cell, ROS reactive oxygen species, SSB single-strand breaks