top of page

NQO1 - Recycles NAD, Detoxes Benzene, Neutralizes Quinones, Stimulates CoQ10 Genes, and host of other things......

This article is not medical advice. Before starting any health related to regimen, seek the advice of your Primary Care Physician or an M.D.

NQO1 from my view is one of the most important genes, for many reasons, but primarily it recycles NAD+, which is one of the most common cofactors in the human system. Below i have highlighted some more of the roles it plays. Its Co-factor ? A favorite, B2:). If you have interest, explore the references at the bottom of the article. If this gene is compromised genetically (not common), its significant, and deserves attention.

NQO1: A brief summary of what this gene does:

  1. Recycles NAD+ by regulating NADP/NADPH ratio

  2. Detoxifies volatile organic compounds like benzene

  3. Scavenges the potent free radical super oxide

  4. Reduces the toxic quinones associated with processing the following :

    1. Caeffeic acid, rosemary, tea, cocao, catechols (dopamine, adrenaline, etc);

    2. Tryptamine (cheese), Ellagic Acid (pomagranate, berries), Luteolin (celery, thyme)

    3. ECGC, cranberry, quercetin (apples), milk thistle, black cummin seed, genistein, resveratrol

  5. Protects against alcohol poisoning

  6. Is involved in protecting the body during the detoxification and breakdown of :

    1. BPA

    2. Estraidol

    3. Tamoxifan

    4. PCB's.

  7. Is key in inducing genes involved in the generation of coq10 (coq9, coq10)

  8. Has a role to play in each of the following:

    1. Alzheimer's Disease

    2. Aging

    3. Insulin / Glucose Regulation

    4. Metabolic Syndrome

    5. Viral replication in HIV, Hepatitis

    6. Protects proteins from proteasomal degradation

    7. Plasma membrane redox system (lipid oxidation)


"The first reported association of NQO1 with microtubules came from studies using Xenopus egg extracts where experiments with inhibitors and immuno depletion showed that inhibition or loss of NQO1 resulted in a decrease in microtubule mitotic structures...... A number of NAD+-dependent enzymes including SIRT2 and PARP have also been observed to co-localize with these acetylated microtubule structures suggesting that NQO1 may be providing NAD+ for these enzymes . More recently it was demonstrated that mitotic progression was delayed when NQO1 was compromised . In these studies, NQO1 and SIRT2 were shown to be bound together and co-localized to the mitotic spindle where it was proposed that NQO1 functions as a downstream modulator of SIRT2 deacetylase activity through its ability to bind to SIRT2 and provide NAD+.

We had previously suggested that binding of oxidized NQO1 to acetylated microtubules could act as a mechanism to retain the enzyme near microtubules where NQO1 could provide antioxidant protection. Given more recent findings, it also seems probable that NQO1 localization on microtubules provides a mechanism to regulate the microtubule acetylome and acetylation/deacetylation balance.

NQO1 may modulate acetylation levels in cells via a number of mechanisms. The notion that NQO1 can generate NAD+ during catalysis to provide NAD+ for SIRT mediated deacetylation has been supported by a number of studies. We did not find evidence for this mechanism in the cellular model systems that we used; however, we found that NQO1 conformation, which is primarily regulated by the redox environment, can result in modulation of acetyl α-tubulin K40 levels and microtubule structure. Therefore, in addition to providing NAD+, NQO1 may also respond to the local pyridine nucleotide redox environment surrounding SIRT2 rich regions of microtubules and modulate the acetylation/deacetylation balance via conformation-dependent protein interactions.

Overall, this emphasizes the redox and conformational-dependent changes in NQO1 structure and how it may play an alternative redox sensing and/or redox-switching role. Changes in pyridine nucleotide redox status would result in altered NQO1 conformation which in turn could modulate downstream NQO1 interactions. Whether conformational changes in NQO1 result in altered location of the protein is intriguing and needs to be further investigated. NQO1 is known to be primarily cytosolic but has been reported to have significant nuclear, mitochondrial and membrane pools in different cell types."[2]

"Flavonoids are plant polyphenolic compounds ubiquitous in fruits, vegetables and herbs. The flavonol quercetin is one of the most abundant dietary flavonoids. It has diverse biological properties in cultured cells, including cytoprotection, and exhibits antitumorigenic effects in animal models. The mechanism(s) for the protective properties of flavonoids are currently unknown but may involve modulation of phase II detoxifying enzymes. We have investigated the effect of quercetin on expression and enzymatic activity of one of the major phase II detoxification systems, NAD(P)H:quinone oxidoreductase (NQO1) in the MCF-7 human breast carcinoma cell line. We show that treatment of MCF-7 cells for 24 h with 15 microM quercetin results in a twofold increase in NQO1 protein levels and enzyme activity, and a three- to fourfold increase in NQO1 mRNA expression. We found that when these cells were transiently transfected with a luciferase (Luc) reporter plasmid containing two copies of the antioxidant response element (ARE) of the human NQO1 gene linked to a minimal viral promoter, quercetin caused an approximately twofold increase in Luc activity. Quercetin failed to increase Luc activity in cells transfected with a reporter vector containing a mutated ARE. The increase in NQO1 transcription in response to quercetin suggests that dietary plant polyphenols can stimulate transcription of phase II detoxifying systems, potentially through an ARE-dependent mechanism. Induction of the human NQO1 gene by dietary polyphenolics could afford protection against carcinogenic chemicals in molecular pathways utilizing the ARE."[7]

"For the alleviation of menopausal symptoms, women frequently turn to botanical dietary supplements, such as licorice and hops. In addition to estrogenic properties, these botanicals could also have chemopreventive effects. We have previously shown that hops and its Michael acceptor xanthohumol (XH) induced the chemoprevention enzyme, NAD(P)H:quinone oxidoreductase 1 (NQO1), in vitro and in vivo. Licorice species could also induce NQO1, as they contain the Michael acceptors isoliquiritigenin (LigC) found in Glycyrrhiza glabra (GG), G. uralensis (GU), and G. inflata (GI) and licochalcone A (LicA) which is only found in GI. These licorice species and hops induced NQO1 activity in murine hepatoma (Hepa1c1c7) cells; hops >> GI > GG ≅ GU. Similar to the known chemopreventive compounds curcumin (turmeric), sulforaphane (broccoli), and XH, LigC and LicA were active dose-dependently; sulforaphane >> XH > LigC > LicA ≅ curcumin >> LigF. Induction of the antioxidant response element-luciferase in human hepatoma (Hep-G2-ARE-C8) cells suggested involvement of the Keap1-Nrf2 pathway. GG, GU, and LigC also induced NQO1 in non-tumorigenic breast epithelial MCF-10A cells. In female Sprague-Dawley rats treated with GG and GU, LigC and LigF were detected in the liver and mammary gland. GG weakly enhanced NQO1 activity in the mammary tissue but not in the liver. Treatment with LigC alone did not induce NQO1 in vivo most likely due to its conversion to LigF, extensive metabolism, and its low bioavailability in vivo. These data show the chemopreventive potential of licorice species in vitro could be due to LigC and LicA and emphasize the importance of chemical and biological standardization of botanicals used as dietary supplements. Although the in vivo effects in the rat model after four day treatment are minimal, it must be emphasized that menopausal women take these supplements for extended periods of time and long-term beneficial effects are quite possible."[8]

"Oxidative stress and neuroinflammation are critical in the pathogenesis of neurodegenerative diseases. Extract of Coreopsis tinctoria Nutt. has been shown to ameliorate neurodegenerative diseases, potentially via inducing quinone oxidoreductase 1 (NQO1) and anti-neuroinflammation. The present study aimed to characterize the chemical profile and bioactive composition of the extract to identify the effective components responsible for the effects. Chromatography and spectra analysis yielded 26 constituents, including a new chalcone (compound 8). Bioassays showed that compounds 6, 9, 15, 17, 19, 21 and 22 significantly inhibited production of nitric oxide (NO) in N9 cells induced by lipopolysaccharides (LPS). Meanwhile compounds 1, 3, 6, 11, 19 and 20 exhibited significant NQO1 inducing activities in Hepa 1c1c7 cells. These results suggest that extract of C. tinctoria Nutt. contains bioactive components attenuating the progress of neurodegenerative diseases, thus, a valuable functional food for the prevention of neurodegenerative diseases."[9]

"Artemisia annua L., which is also known as ‘sweet wormwood’ and ‘Qinghao’, has traditionally been used in China for the treatment of fever and chills . The herb has been reported to contain various bioactive compounds. In particular, artemisinin and its derivatives have been clinically used to treat drug-resistant malaria while they were reported to have several bioactive functions including antitumor and anti-inflammatory activities . In addition, coumarins, flavonoids, and other terpenoids constituents present in A. annua L. are also reported to have significant pharmacological activities such as antitumor and antibacterial activities that contribute to the therapeutic effects of the herb . The total antioxidant capacity (ORAC) of A. annua leaves extract was reported as 1,125 mmoles of Trolox equiv/g, which is half of the ORAC of oregano (the highest reported ORAC for an herb) extracts. Some flavonoids and sesquiterpenes were well known to induce antioxidant and phase 2 detoxifying enzymes such as NAD(P)H:- quinone oxidoreductase 1 (NQO1), heme oxygenase 1, cglutamylcycteine ligase, glutathione reductase and glutathione Stransferase as well as have direct radical scavenging activity . Therefore, A. annua rich in flavonoids and sesquiterpenes is most like to have capability to induce antioxidant enzymes and exert in vivo antioxidative activity. Although in vitro antioxidant potential of A. annua L. extract was reported, the in vivo antioxidant activity of the herbal extract has not been studied so far to our best knowledge...........Induction of NQO1 activity by A. annua extract The enzyme activity of NQO1, one of the antioxidant and anticarcinogenic biomarker enzymes, was dose-dependently induced by AA extract in the range of 12.5 to 200 mg/mL in murine hepatoma hepa1c1c7 cells. The NQO1 activity was increased by ,20% and ,60% in hepa1c1c7 cells treated with the concentrations of 25 and 200 mg/mL of AA extract at both extraction temperatures of room and 80uC, respectively, while the enzyme activity was enhanced by 90% by 10 mM sulforaphane, a well-known NQO1 inducer."[10]


  1. The diverse functionality of NQO1 and its roles in redox control. By David Ross∗ and David SiegelRedox Biol. 2021 May; 41: 101950. Published online 2021 Mar 20. doi: 10.1016/j.redox.2021.101950 . PMCID: PMC8027776. PMID: 33774477

  2. Activation of AhR-NQO1 Signaling Pathway Protects Against Alcohol-Induced Liver Injury by Improving Redox Balance. By Haibo Dong,1,∗ Liuyi Hao,Cell Mol Gastroenterol Hepatol. 2021; 12(3): 793–811. Published online 2021 May 31. doi: 10.1016/j.jcmgh.2021.05.013. PMCID: PMC8340139. PMID: 34082111

  3. The multi-faceted role of NADPH in regulating inflammation in activated myeloid cells Kenneth K. Y. Ting1,2*Jenny Jongstra-Bilen, et. al. Front. Immunol., 30 November 2023 Sec. Nutritional Immunology. Volume 14 - 2023 |. Immunometabolism: Bridging the Gap Between Immunology and Nutrition

  4. Roles of NAD(P)H:quinone Oxidoreductase 1 in Diverse Diseases. by Wang-Soo Lee, Woojin Ham, Life 2021, 11(12), 1301;

  5. Potential Modulation of Human NAD[P]H-Quinone Oxidoreductase 1 (NQO1) by EGCG and Its Metabolites—A Systematic Computational Study. By Pankaj Pandey, Bharathi Avula Cite this: Chem. Res. Toxicol. 2020, 33, 11, 2749–2764. Publication Date:September 25, 2020

  6. Pau d'arco activates Nrf2-dependent gene expression via the MEK/ERK-pathway Michelle Richter 1, Angelika F Winkel, et. al. J Toxicol Science. . 2014 Apr;39(2):353-61. doi: 10.2131/jts.39.353. PMID: 24646717. DOI: 10.2131/jts.39.353

  7. Induction of human NAD(P)H:quinone oxidoreductase (NQO1) gene expression by the flavonol quercetin. L G Valerio Jr 1, J K Kepa, G V Pickwell, L C Quattrochi, et. al. Toxicol Letters. 2001 Feb 3;119(1):49-57. doi: 10.1016/s0378-4274(00)00302-7. PMID: 11275421. DOI: 10.1016/s0378-4274(00)00302-7

  8. Induction of NAD(P)H:quinone oxidoreductase 1 (NQO1) by Glycyrrhiza species used for women's health: differential effects of the Michael acceptors isoliquiritigenin and licochalcone Atieh Hajirahimkhan, Charlotte Simmler, et. al. Chem Res Toxicol. Author manuscript; available in PMC 2016 Nov 16. Chem Res Toxicol. 2015 Nov 16; 28(11): 2130–2141. Published online 2015 Nov 5. doi: 10.1021/acs.chemrestox.5b00310 PMCID: PMC4898475. NIHMSID: NIHMS783012. PMID: 26473469

  9. Anti-neuroinflammatory and NQO1 inducing activity of natural phytochemicals from Coreopsis tinctoria. Ning Li a b, Dali Meng, et. al.

  10. Protective Effect of Artemisia annua L. Extract against Galactose-Induced Oxidative Stress in Mice Mi Hye Kim1 , Ji Yeon Seo. PlosOne. July 2014 | Volume 9 | Issue 7 | e101486.

  11. NQO1 Enzyme and its Role in Cellular Protection; an Insight. By Ahmed Atiaa Iberoamerican Journal of Medicine, vol. 2, núm. 4, pp. 306-313, 2020 Hospital San Pedro. DOI:

3 views0 comments

Recent Posts

See All


bottom of page