Director: Jeffrey Laskin, Ph.D..
Toxicology
The Toxicology Division investigates how environmental exposures contribute to diseases like cancer, birth defects, neurodegeneration, and endocrine disorders. Using diverse analytical methods and EOHSI Core Facilities, faculty conduct cutting-edge research. The division hosts two NIH-funded Centers of Excellence focused on environmental health and chemical threat response, enhancing its scientific impact.
Focus
Research in the Toxicology Division is focused on the nature of human health effects associated with environmental and occupational chemical exposures and the mechanisms by which they occur. Current research emphasizes neurotoxicology, ocular and dermal toxicity, carcinogenesis, oxidative stress, inflammatory mechanisms, development, and xenobiotic metabolism.
Studies on the neurotoxicity of atrazine and its ability to kill dopaminergic neurons.
Neurotoxicology
This research explores oxidative stress mechanisms in a pesticide-based developmental model of Parkinson’s disease using combined paraquat and maneb exposure. Postnatal exposure leads to sustained lipid peroxidation, indicating prolonged oxidative stress. A double-mutant alpha-synuclein transgenic mouse model was developed to study gene-environment interactions and increased vulnerability to these pesticides. Laser capture microdissection and microarray analysis of dopaminergic neurons revealed gene expression changes linked to early exposure. The study also investigates gender differences in neuroprotection, noting female resilience, and examines how prenatal maneb exposure heightens susceptibility to paraquat, offering insights into developmental and genetic risk factors for Parkinson’s disease.
Carcinogenicity
This research investigates environmental and molecular influences on cancer development. Hormone-dependent mammary tumor progression in ACI rats is affected by environmental factors altering antioxidant enzyme expression. A transgenic mouse model reveals that aberrant Grm1 expression in melanocytes induces melanoma. Studies assess how EMMPRIN and collagen XXIII enhance metastasis and help evaluate carcinogenic agents. Additional research explores tobacco smoke carcinogens, UV-induced signal transduction, dietary nutrient inhibitors, and photosensitizer mechanisms. Polyamines and estradiol impact gene expression and protein stability in breast cancer cells, with microarray and CD spectral analysis providing insights into transcriptional regulation and estrogen receptor dynamics.
Division News
