Atrazine, the most widely utilized triazine herbicide in the United States, can leach into groundwater or enter water systems via runoff. The purpose of this experiment is to see if atrazine leads to upregulation of proteins associated with hypoxia induced tumors (fibrosis) in liver tissue. Tumor necrosis factor (TNF-α) is a major component of the signal pathway which leads to liver fibrosis. IKKβ, the major downstream kinase of TNF-α, mediates TNF-α regulation of hypoxia-inducible factor 1-alpha (HIF-1α). This leads to increased expression of vascular endothelial growth factors (VEGF) protein levels. One member of the VEGF family is VEGF-C.  66-six week old male and female mice (Mus musculus) were separated into three treatment groups: 0 ppb+Vehicle (Control), 3 ppb+vehicle (EPA legal limit of atrazine in groundwater), 30 ppb+vehicle (amount found in SE Minnesota watersheds). Mice were given atrazine+vehicle ad libitum for 10 weeks. After 10 weeks, the mice were sacrificed and the liver was extracted. TNF-α, HIF-1α ELISA kits and immunoblot with a VEGF-C antibody were utilized to measure the respective protein concentration in liver tissue.TNF-α protein expression will be correlated with HIF-1α and VEGF-C protein expression to determine the extent of tumor/fibrotic development in mice liver tissue.

Expression of proteins TNF-α and VEGF-C involved in hepatic tumor induction of fibrosis

255th National Meeting (2018)

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