Human AP Endonuclease 1: A Potential Marker for the Prediction of Environmental Carcinogenesis Risk

Table 1

Interference of APE1 upon environmental carcinogen exposure using in vitro and in vivo mammalian models and human population samples.

Environmental factor	Subject	Dose	Effect on APE1	Reference
Heavy metal
Arsenic	Human skin cell line	0.005–5 μM	Decrease of APE1 mRNA expression	[66]
	Human lung cell line	5 μM	Decrease of APE1 mRNA expression	[67]
	Human skin cell line	0.1–5 μM	Increase of APE1 protein expression (short-term)	[68]
		0.1 or 0.5 μM	Decrease of APE1 protein expression (long-term)
		>1 μM	Dose-dependent decrease of APE1 mRNA expression
	Human lung and skin cell lines	<1 μM	Increase of APE1 protein expression	[69]
		5–100 μM	Dose-dependent increase of APE1 mRNA expression
	Mouse embryo cell line	10–75 μM	Dose-dependent increase of APE1 protein expression	[70]
		10–100 μM	Dose-dependent increase of APE1 activity
	Human population	—	Induction of APE1 polymorphism (D148E)	[71]
	Human population	—	Induction of skin lesions with APE1 polymorphism (D148E)	[72]*
	Human kidney cell line	100 μM	No effect on APE1 activity	[73]
Cadmium	Human colon cell line	>10 μM	Decrease of APE1 mRNA expression	[74]
		>25 μM	Decrease of APE1 activity
	Human kidney cell line	100 μM	Decrease of APE1 activity	[73]
	Human population	—	Decrease of APE1 mRNA expression	[75]
	Human breast and cervix cell lines	20–80 μM	No effect on APE1 protein expression and activity	[76]
Lead	Mouse brain cell	10 μM	APE1 accumulation in nucleus	[77]
	Hamster ovary cell line	0.5–500 μM	Dose-dependent accumulation of AP sites and decrease of APE1 activity	[4]
	Human kidney cell line	100 μM	Decrease of APE1 activity	[73]
	Human population	—	Induction of APE1 polymorphism (D148E)	[78]
	Human population	—	No effect on APE1 mRNA expression	[75]
Smoking
	Swiss ICR albino mice	119, 292, 438, 631 mg/m^3 (TSM^§)	Decrease of APE1 protein expression in brain tissue	[79]
	Human population	—	Induction of lung cancer with APE1 polymorphism (D148E and −656T > G)	[80–83]*
	Human population	—	Induction of bladder cancer with APE1 polymorphism (D148E)	[84]*
	Human population	—	No effect on the induction of lung cancer with APE1 polymorphism (D148E)	[85, 86]
	Human population	—	No effect on the induction of bladder cancer with APE1 polymorphism (D148E)	[87]
Radiation
Ultraviolet	SKH-1 hairless mice	5 days a week, 9 h a day at 10,000 lx (UVC)	Increase of APE1 mRNA expression	[88]
	Human lymphocyte	4 J/m^2 (UVA)	Induction of APE1 polymorphism (D148E)	[89]
	Human cervix cell line	0.2 J/cm^2 (UVA)	Induction of APE1 relocalization to nuclear speckles	[90]
Ionizing radiation	Human population	—	Induction of APE1 polymorphism (D148E)	[91]
	Human population	—	Induction of breast cancer with APE1 polymorphism (D148E)	[92]
	Human population	—	Induction of APE1 polymorphism (D148E)	[93]
	Human lung cell line	200 cGy/min (X-ray)	Increase of APE1 protein expression	[94]
	Human lung cell line	4, 16 Gy (X-ray)	Increase of APE1 protein expression	[95]
	Human blood culture	80 cGy/min (X-ray)	Induction of APE1 polymorphism (D148E)	[89]
	Human lymphocyte	1 Gy/min (X-ray)	Induction of APE1 polymorphism (D148E)	[96]

*It represents study of gene-environment interaction; ^§TSM is abbreviation of total suspended matter in average after burning cigarette.