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Current Toxicology Scholars
Suren Bandara

I am a PhD student in the Neuroscience Program. My research focus is on developmental environmental contaminant exposures and how it may affect auditory function in adulthood, using a rat model. Under the mentorship of Dr. Susan Schantz, I have been studying the effects of Polychlorinated Biphenyls (PCBs) on auditory function, with recent focus on how PCB exposure may also cause audiogenic seizures. My experiments are geared towards understanding the mechanism behind PCB induced audiogenic seizures at the level of the brainstem and to recognize if PCB exposure during development would facilitate electrically induced seizures (kindling). I hypothesize that rats exposed to higher doses of PCBs will be more susceptible to audiogenic seizures and will likely be susceptible to the more generalized electrically kindled seizures. These studies may lead to the recognition of human populations with increased seizure susceptibility due to the consumption of PCB contaminated fish.
Patrick Hannon
Comparative Biosciences



I am a Ph.D. student in Dr. Jodi Flaws’ laboratory in the Department of Comparative Biosciences. My current research focuses on how environmental chemicals impact normal ovarian function. Specifically, I am interested in how the common plasticizer di(2-ethylhexyl) phthalate (DEHP), a known endocrine disrupting chemical, affects ovarian follicular development and functions such as steroidogenesis. I am interested in studying the effects of DEHP on folliculogenesis and steroidogenesis because any alteration in these processes can be detrimental to fertility. Additionally, ovarian derived steroid hormones play important roles in non-reproductive physiology such as cardiovascular and skeletal health, thus highlighting the importance in studying the effect of DEHP on steroid hormone production. Based on earlier work from other members of Dr. Flaws’ group and me, we have determined that DEHP negatively affects both of these vital processes by accelerating early folliculogenesis and decreasing the levels of estradiol. I hypothesize that DEHP interferes with intraovarian factors responsible for early folliculogenesis and that DEHP affects both precursor hormones and enzymes responsible for generating estradiol.  My goal is to continue to utilize both in vivo and in vitro systems to understand the mechanism by which environmentally relevant levels of DEHP affect normal ovarian folliculogenesis and steroidogenesis.

Liang Ma
Materials Science & Engineering



I am a PhD candidate in Department of Materials Science and Engineering. My current research is focused on nanoparticles-mediated environmental toxicity study, especially Quantum dots (QDs). QDs, tiny light-emitting nanocrystals, show great potential as alternative fluorescent probes due to several significant advantages over conventional molecular fluorophores, including size and composition tunable light emission, improved brightness, excellent photo-stability, and multicolor fluorescence with a single-wavelength excitation. In the past decade, tremendous research efforts have been made to synthesize high quality QDs for in vitro and in vivo imaging. However, potential toxicity of QDs from long-term release of toxic elements (Cd, Hg, Pb, Se, As, etc.) remains a major roadblock to clinical translation. In addition, there are significant environmental concerns regarding the use and disposal of heavy-metal contained QDs. I have two primary research goals: to prepare nontoxic QDs for translation into clinical applications and to use QDs as a sensitive probe for understanding the mechanisms of nanoparticle-mediated toxicity in vivo. Under the supervision of Dr. Andrew Smith in Department of Bioengineering, I will pursue these objectives through the following specific aims. Aim 1 focuses on preparing nontoxic QDs and studying the toxicity of core materials in vitro. Aim 2 introduces compact surface coatings to maximize renal clearance of QDs. Aim 3 systematically explores biodistribution and pharmacokinetics of compact QDs. I hope my research will develop novel nontoxic QDs with compact surface coatings that can be potentially translated into clinical applications. Also, biodistribution and pharmacokinetics of nanoparticles with hydrodynamic diameters in 4 – 10 nm will be systematically studied for the first time.

Changqing Zhou
Comparative Biosciences


I am a Ph.D. Student in Dr. Jodi Flaws’ laboratory in the department of Comparative Biosciences. My research is focusing on how endocrine disrupting chemicals impact normal ovarian functions. Specifically, I am testing the ovotoxicity of a phthalate mixture made from six phthalates commonly found in humans. Most previous toxicity studies have focused on a single chemical or a mixture of chemicals that do not reflect the human exposure levels. My study will be the first to test the toxicity of a phthalate mixture made according to human exposure in an environmentally relevant dose range. Further, I will study the impact of the chemical exposure on the first and subsequent generations. This will provide information on the transgenerational effects of chemical exposure. 

Azra Dad
Crop Sciences


I am a PhD student in Dr. Michael Plewa’s lab in the department of Crop sciences. My research project is about the toxicity mechanism of regulated and non-regulated halogenated water disinfection by-products (DBPs) including mono, di, and tri haloacetic acids (HAAs). In chlorinated water the second largest DBP chemical class is the HAAs. Based on the literature from different labs including ours, HAAs are alkylating agents and highly cytotoxic, genotoxic, mutagenic, teratogenic and carcinogenic. My hypothesis is that monoHAAs inhibit glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a target cytosolic enzyme. The HAAs induced GAPDH inhibition will lead to a severe reduction of cellular ATP levels and repress the generation of pyruvate. A loss of pyruvate will lead to mitochondrial stress and generation of reactive oxygen species (ROS) due to the insufficiency of reducing power (NADH). The ROS generated by mitochondria will lead to oxidative DNA damage but supplementing cells with exogenous pyruvate should rescue the cells against the HAAs mediated stress (oxidative DNA damage and reduction in ATP levels). Exogenous supplementation with pyruvate enhanced cellular ATP levels and attenuated monoHAAs induced genomic DNA damage as measured with single cell gel electrophoresis. These data were highly correlated with the SN2 alkylating potentials of the monoHAAs and with the induction of toxicity. The results from this study strongly support the hypothesis that GAPDH inhibition and subsequent generation of reactive oxygen species is linked with the cytotoxicity, genotoxicity, teratogenicity, and neurotoxicity of these DBPs. However, my research has shown that the mechanism of action for the di and triHAAs is different than the monoHAAs because these HAAs have a different target molecule. Studies have shown that pyruvate supported calcium transportation in mitochondria and pyruvate dehydrogenase activation are coupled activities and play a major role in cellular calcium homeostasis and ATP production. Moreover, dichloroacetic acid activates pyruvate dehydrogenase by inhibiting the pyruvate dehydrogenase kinase. I postulate that increased activation of PDH activity by diHAAs and triHAAs accelerates the release of pyruvate, lactate and alanine from cells which in turn disturbs the glucose homeostasis and leads to toxicity. The chronic exposure to diHAAs and triHAAs through drinking water may be involved with hypolactatemia, disturbed glucose homeostasis and hepatotoxicity in humans especially sensitive populations (featuses).