Table 2.

Main features of experimental models for study of ROS-related pathological processes

Models	Mechanisms	Main features	Application	References
Ras	NOX activation Mitochondria?	Chromosome remodeling, p53, p16 activation, ROS increase, altered redox	ROS in cancer & senescence	2–8
Bcr-Abl	NOX? Mitochondria?	Increased ROS, chromosomal fragmentation, DNA damage, decreased PTPase activity	Leukemia (CML)	8, 10–12
C-myc	Mitochondria Other?	Increased ROS, DNA damage, increased genomic instability	Various cancer	14–16
p53	Mitochondria glycolysis, PPP	Alter redox homeostasis, SCO2, TIGAR, SESN1/2, PIG3, Puma, BAX activation	Longevity, ageing, cancer, apoptosis	18–19,21, 42,44
SOD1	Affect O2− elimination	Abnormal mitochondria, oxidative DNA and protein damage	Cancer, ageing, neurodegeneration	22–26
SOD1G93ATG	Gain of toxic function	Protein carbonylation and aggregation, ROS increase, abnormal mitochondria	ALS	27–29
SOD2+/−	Mitochondrial ROS↑	ROS increase, nDNA & mtDNA damage, altered mitochondria	Cancer	32
SOD2−/−	Mitochondrial ROS	Fe-S protein function loss, DNA oxidation, metabolic alteration, ROS	Role of ROS in cancer & development	30–31
SOD3TG	↓ extracellular O2−	Decrease in oxidative DNA damage	ROS in skin cancer	34
Catalase	Lower ROS	Decreased ROS and mtDNA damage protected aconitase function	Role of mitochondrial ROS in longevity	35
GPX1	Redox alteration	Aberrant ROS and RNS responses	Cancer, diabetes	39–41