Lei Guo Ph.D.

Research Biologist — Division of Biochemical Toxicology

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Lei Guo, Ph.D.
(870) 543-7121
NCTRResearch@fda.hhs.gov

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Background

Lei Guo received a Ph.D. in molecular biology from the University of Tokyo (Japan) and worked as a postdoctoral fellow and then as a research assistant professor at the University of Alberta (Canada) for four years. Dr. Guo joined FDA’s National Center for Toxicological Research (NCTR) in 2003 as a research biologist. She has published >100 articles in peer-reviewed journals and 16 book chapters. Her work has been cited more than 4,000 times.

Research Interests

Dr. Guo's research focuses on mechanistic studies of drug- and herbal dietary supplement-associated toxicities. She uses multiple in vitro models and approaches, including, but not restricted to, molecular and biochemical methods, genomic analyses, and in silico molecular docking for evaluation and prediction of toxicity and elucidation of toxic mechanisms. Her research results demonstrate that this combined approach is useful for hazard identification and that in-depth molecular mechanistic studies can provide toxicological information for FDA-relevant products.

Professional Societies/National and International Groups

International Agency for Research on Cancer/World Health Organization Monographs on the Evaluation of Carcinogenic Risks to Humans
Committee member
2013 and 2020

National Institute of Environmental Health Sciences P42 Superfund
Grant Review Member
2019

Society of Toxicology (SOT)
Member
2019 – 2023

Board of Publication, SOT
Co-chair
2021

Regional Chapter Collaboration and Communication Committee Undergraduate Award Selection Committee, SOT
Member
2018

South Central Chapter, SOT
Secretary
2011 – 2016

Selected Publications

A Mechanism of Perhexiline's Cytotoxicity in Hepatic Cells Involves Endoplasmic Reticulum Stress and P38 Signaling Pathway.
Ren Z., Chen S., Park S., and Guo L.
Chem Biol Interact. 2021, 334:109353. doi: 10.1016/j.cbi.2020.109353

Characterization of Cytochrome P450s (CYP)-overexpressing HepG2 Cells for Assessing Drug and Chemical-Induced Liver Toxicity.
Chen S., Wu Q., Li X., Li D., Mei N., Ning B., Montserrat P., Ren Z., William H., and Guo L.
J Environ Sci Health C Toxicol Carcinog. 2021, 39(1):68-86. doi: 10.1080/26896583.2021.1880242

Roles of CYP3A4, CYP3A5 and CYP2C8 Drug-Metabolizing Enzymes in Cellular Cytostatic Resistance.
Hofman J., Vagiannis D., Chen S., and Guo L.
Chem Biol Interact. 2021, 340:109448. doi: 10.1016/j.cbi.2021.109448

Mitochondrial Dysfunction and Apoptosis Underlie the Hepatotoxicity of Perhexiline.
Ren Z., Chen S., Seo JE., Guo X., Li D., Ning B., and Guo L.
Toxicol In Vitro.2020, 69:104987. doi: 10.1016/j.tiv.2020.104987

The Role of Hepatic Cytochrome P450s in the Cytotoxicity of Sertraline.
Chen S., Wu Q., Li X., Li D., Fan M., Ren Z., Bryant M., Mei N., Ning B., and Guo L.
Arch Toxicol. 2020, doi: 10.1007/s00204-020-02753-y.

The Role of Hepatic Cytochrome P450s in the Cytotoxicity of Dronedarone.
Chen S, Wu Q, Ning B, Bryant MS, Guo L.
Arch Toxicol. 2018, 96 (6):1969-1981. doi:10.1007/s00204-018-2196-x

Mitochondrial Dysfunction Induced by Leflunomide and its Active Metabolite.
Xuan J., Ren Z., Qing T., Couch L., Shi L., Tolleson WH., Guo L.
Toxicology. 2018, 396: 33-45. doi: 10.1016/j.tox.2018.02.003.

DNA Damage-Induced Apoptosis and Mitogen-Activated Protein Kinase Pathway Contribute to the Toxicity of Dronedarone in Hepatic Cells.
Chen S., Ren Z., Yu D., Ning B., Guo L.
Environ Mol Mutagen. 2018, 59:278-289. doi: 10.1002/em.22173.

Endoplasmic Reticulum Stress and MAPK Signaling Pathway Activation Underlie Leflunomide-Induced Toxicity in HepG2 Cells.
Ren Z., Chen S., Qing T., Xuan J., Couch L., Yu D., Ning B., Shi L., Guo L.
Toxicology. 2017, 392:11-21. doi: 10.1016/j.tox.2017.10.002.

Activation of the Nrf2 Signaling Pathway in Usnic Acid-Induced Toxicity in HepG2 Cells.
Chen S., Zhang Z., Qing T., Ren Z., Yu D., Couch L., Ning B., Mei N., Shi L., Tolleson W., and Guo L.
Arch Toxicol. 2017, 91:1293-1307. doi: 10.1007/s00204-016-1775-y.

The Role of CYP 3A4 and 1A1 in Amiodarone-Induced Hepatocellular Toxicity.
Wu Q., Ning B., Xuan J., Ren Z., Guo L., and Bryant M.
Toxicol Lett. 2016, 253:55-62. doi: 10.1016/j.toxlet.2016.04.016.

Development of HepG2-Derived Cells Expressing Cytochrome P450s for Assessing Metabolism-Associated Drug-Induced Liver Toxicity.
Xuan J., Chen S., Ning B., Tolleson W., and Guo L.
Chem Biol Interact. 2016, 5: 63-73. doi: 10.1016/j.cbi.2015.10.009.

Endoplasmic Reticulum Stress and Store-Operated Calcium Entry Contribute to Usnic Acid-Induced Toxicity in Hepatic Cells.
Chen S., Zhang Z., Wu Y., Shi Q., Yan H., Mei N., Tolleson W., and Guo L.
Toxicol Sci. 2015, 146:116-126. doi: 10.1093/toxsci/kfv075.

The Role of Autophagy in Usnic Acid-Induced Toxicity in Hepatic Cells.
Chen S., Dobrovolsky V., Liu F., Wu Y., Zhang Z., Mei N., and Guo L.
Toxicol Sci. 2014, 142:33-44. doi: 10.1093/toxsci/kfu154.

Sertraline Induces Endoplasmic Reticulum Stress in Hepatic Cells.
Chen S., Xuan J., Couch L., Iyer A., Wu Y., Li Q., and Guo L.
Toxicology. 2014, 322C:78-88. doi: 10.1016/j.tox.2014.05.007.

Sertraline, an Antidepressant, Induces Apoptosis in Hepatic Cells through the Mitogen-Activated Protein Kinase Pathway.
Chen S., Xuan J., Wan L., Lin H., Couch L., Mei N., Dobrovolsky V., and Guo L.
Toxicol Sci. 2014, 137:404-415. doi: 10.1093/toxsci/kft254.

Mechanism Study of Goldenseal-Associated DNA Damage.
Chen S., Wan L., Couch L., Lin H., Li Y., Dobrovolsky V., Mei N., and Guo L.
Toxicol Lett. 2013, 221:64-72. doi: 10.1016/j.toxlet.2013.05.641.

Mitochondrial Dysfunction Induced by Sertraline, an Antidepressant Agent.
Li Y., Couch L., Higuchi M., Fang J., and Guo L.
Toxicol Sci. 2012, 127:582-591. doi: 10.1093/toxsci/kfs100.

Similarities and Differences in the Expression of Drug-Metabolizing Enzymes between Human Hepatic Cell Lines and Primary Human Hepatocytes.
Guo L., Dial S., Shi L., Branham W., Liu J., Fang J., Green B., Deng H., Kaput J., and Ning B.
Drug Metab Dispos. 2011, 39:528-538. doi: 10.1124/dmd.110.035873.

Methysticin and 7,8-Dihydromethysticin Are Two Major Kavalactonesin Kava Extract to Induce CYP1A1.
Li Y., Mei H., Wu Q., Zhang S., Fang J., Shi L., and Guo L.
Toxicol Sci. 2011, 124:388-399. doi: 10.1093/toxsci/kfr235.

Lab Members

Contact information for all lab members:
(870) 543-7121
NCTRResearch@fda.hhs.gov

Si Chen, Ph.D.
Staff Fellow

Yuxi Li, Ph.D.
FDA Staff Fellow

Zhen Ren, Ph.D.
Staff Fellow

Contact Information: Lei Guo; (870) 543-7121