Mar 06, 2024
NQO1 (NAD(P)H QUINONE DEHYDROGENASE 1)
The NQO1 enzyme is found in humans and is encoded by the NQO1 gene. NQO1 is a phase 2 detoxification enzyme that converts reactive quinones to hydroquinones via a two-electron transfer mechanism. In other words, NQO1 is a cytosolic flavoprotein and facilitates the detoxification and excretion of endogenous and exogenous chemicals through the reduction reaction from quinones to hydroquinones (Nioi et al., 2004).
Induction of NQO1 in cells reduces the risk of DNA damage by preventing free radical formation mediated by single electron transfer. It is a protective antioxidant agent, versatile cytoprotective agent. NQO1 regulates oxidative stress of chromatin-binding proteins for DNA damage in cancer cells (Preethi et al., 2022). A study reported that NQO1-/- mice were more susceptible to chemically induced mouse skin carcinogenesis (Long et al., 2001).
Expression and activity of NQO1 are negatively regulated by specific components of pro-inflammatory signaling pathways. In another study, stimulation of cholangiocarcinoma cells with a mixture of cytokines resulted in decreased NQO1 expression (Prawan et al., 2009).
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Phase 2- NQO1 (NAD(P)H quinone dehydrogenase 1) |
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Gene |
rs-code |
Minor Allele |
Minor Allele Description |
Referans |
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NQO1 |
rs1800566 |
T |
Increased relative risk for quinone and benzene toxicity due to decreased enzyme activity. |
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The table above contains the NQO1 (NAD(P)H quinone dehydrogenase 1 gene and its polymorphism. This polymorphism is a genetic variant that may predispose a person to certain conditions or protect a person against certain conditions. The study on this gene is as follows; The NQO1 gene shows that it is an important risk factor in the development of bladder cancer with its rs1800566 polymorphism (Hemissi et al., 2021). This shows us that the genetic polymorphisms people have may create a predisposition to diseases. Therefore, people can predict and prevent these risks by having genetic testing. They can prevent them from getting sick by regulating their lifestyle.
REFERENCES
Hemissi, I., Ayed, H., Naimi, Z., Meddeb, K., Ayadi, M., Zouari, S., Zaghbib, S., Talbi, E., Chebil, M., & Ouerhani, S. (2021). Polymorphisms in NQO1 and MPO genes and risk for bladder cancer in Tunisian population. Molecular Genetics & Genomic Medicine, 9(11), e1819. https://doi.org/https://doi.org/10.1002/mgg3.1819
Long, D. J., Waikel, R. L., Wang, X. J., Roop, D. R., & Jaiswal, A. K. (2001). NAD (P) H: quinone oxidoreductase 1 deficiency and increased susceptibility to 7, 12-dimethylbenz [a]-anthracene-induced carcinogenesis in mouse skin. Journal of the National Cancer Institute, 93(15), 1166-1170. https://academic.oup.com/jnci/article/93/15/1166/2519411
Nioi, P. ve Hayes, JD (2004). NAD (P) H: kinon oksidoredüktaz 1'in karsinojeneze karşı korumaya katkısı ve geninin Nrf2 temel bölge lösin fermuarı ve arilhidrokarbon reseptörü temel sarmal-ilmek-sarmal transkripsiyon faktörleri tarafından düzenlenmesi. Mutasyon Araştırması/Mutajenezin Temel ve Moleküler Mekanizmaları , 555 (1-2), 149-171. https://www.sciencedirect.com/science/article/pii/S0027510704002891
Prawan, A., Buranrat, B., Kukongviriyapan, U., Sripa, B., & Kukongviriyapan, V. (2009). Inflammatory cytokines suppress NAD (P) H: quinone oxidoreductase-1 and induce oxidative stress in cholangiocarcinoma cells. Journal of cancer research and clinical oncology, 135, 515-522. https://link.springer.com/article/10.1007/s00432-008-0483-2
Preethi, S., Arthiga, K., Patil, A. B., Spandana, A., & Jain, V. (2022). Review on NAD(P)H dehydrogenase quinone 1 (NQO1) pathway. Molecular Biology Reports, 49(9), 8907-8924. https://doi.org/10.1007/s11033-022-07369-2