Reinhold J. Hutz
Reinhold J. Hutz
Reproductive Physiology

B.S., Loyola Univ. of Chicago 1978
M.S., Loyola Univ. of Chicago 1980
Ph.D., Michigan State Univ. 1983

Postdoctoral Research Associate
Wisconsin Regional Primate
Research Center, 1983-1986

Office: Lapham N509
Phone: 414-229-5416
FAX: 414-229-3926
Personal Homepage:

Research Interests

My research over the past 20 years has focused upon the reproductive effects of estrogens (natural and environmental pollutants with estrogenic activity) and pollutants that modulate the estrogen-receptor signaling pathway (e.g., dioxin). Such molecules can inhibit ovarian function and fertility in several mammals (including monkeys and women), fish, and aquatic invertebrate species. The following is a more detailed synopsis of my research efforts.

Overall my interests lie in the area of control of development and atresia (apoptotic degeneration) of ovarian follicles in animals (invertebrates, fish, rats, hamsters, guinea pigs, primates). My laboratory evaluates effects of estrogens, follicle-stimulating hormone, growth factors, and nanoparticles on the induction of atresia, studied in vivo and on follicle cells and oocytes in vitro; and the regulation of estrogen receptor function and fertility by endocrine-disrupting pollutants such as dioxins. Techniques utilized are laparotomy, cell culture, histology/histochemistry of fixed and frozen sections, fluorescence microscopy, autoradiography, radioimmunoassay, enzyme assays, image analysis, and various molecular techniques.

In a typical human menstrual cycle, one ovarian follicle (containing a healthy egg cell) from a cohort of a dozen or so goes on to ovulate, relegating the others to degeneration, or atresia by apoptosis. The primary focus of our laboratory is the elucidation of those factors involved in the regulation of ovarian follicle development (folliculogenesis), atresia, and ovulation in mammals. We are particularly intrigued in the role played by estrogens in this process. We have previously shown that administration of estrogens or molecules that alter the estrogen-signaling pathway, induces apoptosis of the dominant follicle(s) in several species in vivo, and inhibits steroid synthesis by components of the follicle in vitro, operating at various enzymatic levels. Some of this inhibitory effect is mediated at the level of the hypothalamus and pituitary of the brain, and some directly at the level of the ovary. These biomedical models strongly suggest that there exits a complicated network of factors involved in overall regulation of folliculogenesis, including steroids, growth factors (such as nerve growth factor), cytokines, peptide hormones, xenobiotics (e.g., dioxins) and angiogenic factors, such as angiotensin II.

The various biomedical models that we use are applicable to humans, but possess the advantages of smaller size, ability to manipulate, genetics (e.g., zebrafish), direct extrapolation (non-human primates), and fewer ethical concerns. The biomedical goals of our studies are to determine the effects of natural and environmental molecules to which we are exposed on a daily basis on reproductive health and fertility in women; and to discern how these detrimental effects may be ameliorated/abolished or prevented.

Selected Publications

Stelzer RV, Hutz RJ. Gold nanoparticles enter rat ovarian granulosa cells and subcellular organelles, and alter in-vitro estrogen accumulation. J Reprod Develop 55:6, 2009 (in press).

T. King Heiden, C. Struble, M. Hessner, R.J. Hutz, and M.J. Carvan, III. Molecular targets of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) within the zebrafish ovary: Insights into TCDD’s reproductive toxicity. Reprod Toxicol 25:47-57, 2008.

Hutz RJ, Carvan MJ III, Baldridge MG, Conley LK, King Heiden T. Environmental toxicants and effects on female reproductive function. Trends in Reproductive Biology Vol. 2:1-11, 2006/07 (also NIH PubMed Central).

Baldridge MG, Hutz RJ. Autoradiographic localization of aromatic hydrocarbon receptor (AHR) in rhesus monkey ovary. Amer J Primatol 69:681-691, 2007.

Trewin AL, Woller M, Wimpee BA, Conley LK, Baldridge MG, Hutz RJ. Short-term hormone release from adult female rat hypothalamic and pituitary explants is not altered by 2,3,7,8-tetrachlorodibenzo-p-dioxin. J Reprod Develop 53:765-775, 2007.

Ho HM, Ohshima K, Watanabe G, Taya K, Strawn EY, Hutz RJ. TCDD increases inhibin A production by human luteinized granulosa cells in vitro. J Reprod Develop 52:523-528, 2006 (also NIH PubMed Central).

King Heiden T, Carvan MJ III, Hutz RJ. Inhibition of follicular development, vitellogenesis, and serum 17beta estradiol concentrations in zebrafish following chronic, sublethal dietary exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicol Sci 90:490-499, 2006.

Wang T, Huo YJ, Shi FX, Xu RJ, Hutz RJ. Effects of Intrauterine Growth Retardation on Development of the Gastrointestinal Tract in Neonatal Pigs. Biol Neonate 88:66-72, 2005.

King Heiden T, Hutz RJ, Carvan III MJ. Accumulation, tissue distribution, and maternal transfer of dietary 2,3,7,8-tetrachlorodibenzo-p-dioxin: impacts on reproductive success of zebrafish. Toxicol Sci 87:497-507, 2005.

Baldridge MG, Gerstenberger SL, Tripoli V, Stahl R, Hutz RJ. Modulation of ovarian follicle maturation in Long-Evans rats exposed to ammonium perchlorate in utero and lactationally. Reprod Toxicol 19:155-161, 2004.

Baldridge MG, Stahl RL, Gerstenberger SL, Tripoli V, Hutz RJ. Modulation of ovarian follicle maturation in Long-Evans rats exposed to polychlorinated biphenyls in utero and lactationally. Reprod Toxicol 17:567-573, 2003.

Dasmahapatra AK, Trewin AL, Hutz RJ. Estrous cycle-regulated expression of CYP1B1 mRNA in the rat ovary. Comp. Bioch. Physiol. Part B, Bioch Molec Biol. 133:127-134, 2002.