Degree Name
MS (Master of Science)
Program
Biology
Date of Award
12-2018
Committee Chair or Co-Chairs
Yongke Lu
Committee Members
Allan Forsman, Jonathan Peterson, Gary Wright
Abstract
Cadmium is present in food and groundwater. Tobacco smoking and occupational exposure are also major sources for cadmium. Cadmium is primarily accumulated in liver, a major organ metabolizing exogenous chemicals. Chemical metabolism may cause detoxification, but it can also cause bio-activation resulting in liver damage. Cytochrome P450s (CYP) are major liver metabolism enzymes, and cadmium chloride (CdCl2) can induce CYP2A5 in mice. We examined the effect of CYP2A5 on CdCl2-induced liver injury using CYP2A5-knockout (cyp2a5-/-) mice. The cyp2a5-/- mice and their control WT mice were injected CdCl2 intraperitoneally at 5 mg/kg body weight, respectively, to induce liver injury. The control group of cyp2a5-/- mice and WT mice were injected saline at the same volume. Twenty-four hours later, all the mice were sacrificed. As indicated by biochemical assays and pathological evaluation, CdCl2-treated WT mice exhibited more severe liver injury than CdCl2-treated cyp2a5-/- mice, suggesting that CYP2A5 contributes to Cd-induced liver injury.
Document Type
Thesis - unrestricted
Recommended Citation
Salamat, Julia, "The Role of CYP2A5 in Cadmium-Induced Liver Injury" (2018). Electronic Theses and Dissertations. Paper 3498. https://dc.etsu.edu/etd/3498
Copyright
Copyright by the authors.