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.
Identifer | oai:union.ndltd.org:ETSU/oai:dc.etsu.edu:etd-4948 |
Date | 01 December 2018 |
Creators | Salamat, Julia |
Publisher | Digital Commons @ East Tennessee State University |
Source Sets | East Tennessee State University |
Language | English |
Detected Language | English |
Type | text |
Format | application/pdf |
Source | Electronic Theses and Dissertations |
Rights | Copyright by the authors. |
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