|
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/m3 (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/m2 (UVA) | Induction of APE1 polymorphism (D148E) | [89] |
Human cervix cell line | 0.2 J/cm2 (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] |
|