Dr. Craig is an Assistant Professor of Reproductive Physiology in the School of Animal and Comparative Biomedical Sciences within the College of Agriculture and Life Sciences of The University of Arizona since 2013. She has a strong background in physiology, reproduction, and toxicology and has worked in the field of reproductive physiology and toxicology for ten years. Throughout the years, she has conducted research aimed at understanding the relationship between environmental exposures and ovarian function and disease.
Dr. Craig joined the University of Arizona Cancer Center earlier this year when she was identified as a young investigator conducting research that aligns with the center. As a graduate student, she completed work aimed at elucidating the role of the residual ovarian tissue of postmenopausal ovaries on chemically-induced ovarian neoplasms.
Currently, Dr. Craig is investigating how phthalate exposures interact with pathways critical for cell cycle, apoptosis, and DNA damage response pathways in the ovary. Specifically, her work focuses on how the endocrine disruptor dibutyl phthalate and its ability to downregulate the expression of the ovarian cancer susceptibility gene, Brca1. This work is directly related to the Center’s efforts to understand the biology of cancer and expand this understanding to include the effects of the environment on this disease. As a junior faculty member, membership in the Center has allowed her to meet outstanding scientists who have given her valuable career development advice and with whom she hopes to establish collaborations. The Center's Core Facilities represent a valuable resource for junior faculty seeking to incorporate new technologies in their research programs.
Infertility is the inability to produce life offspring. Several factors increase a female’s risk for infertility including aging, stress, and exposure to chemicals. Unfortunately, fertility in women and animals have declined significantly over several decades. Therefore, understanding how these factors influence human and animal fertility are of great health and economic importance.
A group of chemicals collectively known as phthalates have been classified as endocrine disruptors based on their ability to interact with the reproductive system. Phthalates have been detected in human urine, animal tissues, and feed. Despite these observations, knowledge about how phthalates interact with the female reproductive system is currently very limited.
Dr. Craig's work focuses on understanding how phthalates affect the function of the ovary, the major reproductive organ in females. Thus, work in her laboratory is focused on using animal models to help us understand the mechanisms by which phthalates exert their effects on the ovary, determine whether phthalates cause female infertility, and examine whether the effects of phthalates on female reproduction can be prevented or reversed. Using this knowledge she hopes to develop additional models to evaluate other chemicals and environmental factors that could influence both human and animal reproduction.
- Rivera Z, Christian PJ, Marion SL, Brooks HL, Hoyer PB. Steroidogenic capacity of residual ovarian tissue in VCD-treated mice. Biol Reprod 2009; 80:328-336.
- Craig ZR, Davis JR, Marion SL, Barton JK, Hoyer PB. 7,12-dimethylbenz[a]anthracene (DMBA) induces Sertoli-Leydig cell tumors in the follicle-depleted ovary of 4-vinylcyclohexene diepoxide (VCD)-treated mice. Comp Med 2010; 60:10-17.
- Craig ZR, Leslie TL, Hatfield KL, Gupta RK, Flaws, JA. Mono-hydroxy methoxychlor alters levels of key sex steroids and steroidogenic enzymes in cultured mouse antral follicles. Toxicol Appl Pharmacol 2010; 249(2):107-113.
- Wang W, Craig ZR, Basavarajappa MS, Gupta R, Flaws JA. Di (2-ethylhexyl) phthalate inhibits growth of ovarian antral follicles through an oxidative stress pathway. Toxicol Appl Pharmacol 2012; 258:288-295.
- Peretz J, Craig ZR, Flaws JA. Bisphenol A inhibits follicle growth and induces atresia in cultured mouse antral follicles independently of the genomic estrogenic pathway. Biol Reprod. 2012; 87(3):63, 1-11.
- Wang W, Craig ZR, Basavarajappa MS, Hafner KS, Flaws JA. Mono (2-ethylhexyl) Phthalate Induces Oxidative Stress and Inhibits Growth of Mouse Ovarian Antral Follicles. Biol Reprod. 2012; 87(6):152.
- Craig ZR, Hannon PR, Wang W, Ziv-Gal A, Flaws JA. Di-n-butyl phthalate disrupts the expression of genes involved in cell cycle and apoptotic pathways in mouse ovarian antral follicles. Biol Reprod 2013; 88(1):23.