Dominican University of California
 

Presentation or Panel Title

Effects of Chronic Cadmium Exposure on Antioxidant Defense in Breast Cancer Cells

Location

Guzman 202, Dominican University of California

Start Date

4-20-2017 1:35 PM

End Date

4-20-2017 2:00 PM

Department

Natural Sciences and Mathematics

Student Type

Undergraduate - Honors

Faculty Mentor

Maggie Louie, Ph.D. and Shona Mookerjee, Ph.D.

Presentation Format

Oral Presentation

Abstract/Description

Cadmium, a heavy metal and carcinogen, is an environmental contaminant. Human exposure to cadmium can occur via contaminated food, water, and smoking. Cadmium functions as a metalloestrogen and mimics estrogen by binding and activating the estrogen receptor. To understand how chronic exposure to low levels of cadmium affects breast cancer progression, our lab previously demonstrated that cells chronically exposed to cadmium exhibit more metastatic phenotypes like an increase in growth rate, migration, and invasion abilities. Furthermore, our lab previously demonstrated in a microarray analysis that genes induced by oxidative stress imposed by hydrogen peroxide were also induced by chronic cadmium exposure. Therefore, exposure to cadmium may induce oxidative stress-dependent transcription that promotes breast cancer progression. We measured the growth rates of the MCF7 parent line and MCF7-Cd in order to statistically compare their doubling times and found that they were significantly different. We next examined the antioxidant defense systems of these cells to determine whether cadmium exposure inhibited the cell’s normal antioxidant activity and thereby induces transcriptional change. Two different assays were performed to evaluate the effects of chronic cadmium exposure on ROS (reactive oxidative species) neutralization. Cadmium is a known disruptor of glutathione (GSH), binding directly to GSH and preventing it from neutralizing reactive oxygen and nitrogen species. Additionally, superoxide dismutase (SOD) activity was measured since it is known to aid in the cellular antioxidant defense mechanism. We hypothesized that GSH levels and SOD activity would decrease as a result of chronic cadmium exposure. These results will demonstrate whether cadmium-induced oxidative stress could occur through inadequate ROS neutralization.

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Apr 20th, 1:35 PM Apr 20th, 2:00 PM

Effects of Chronic Cadmium Exposure on Antioxidant Defense in Breast Cancer Cells

Guzman 202, Dominican University of California

Cadmium, a heavy metal and carcinogen, is an environmental contaminant. Human exposure to cadmium can occur via contaminated food, water, and smoking. Cadmium functions as a metalloestrogen and mimics estrogen by binding and activating the estrogen receptor. To understand how chronic exposure to low levels of cadmium affects breast cancer progression, our lab previously demonstrated that cells chronically exposed to cadmium exhibit more metastatic phenotypes like an increase in growth rate, migration, and invasion abilities. Furthermore, our lab previously demonstrated in a microarray analysis that genes induced by oxidative stress imposed by hydrogen peroxide were also induced by chronic cadmium exposure. Therefore, exposure to cadmium may induce oxidative stress-dependent transcription that promotes breast cancer progression. We measured the growth rates of the MCF7 parent line and MCF7-Cd in order to statistically compare their doubling times and found that they were significantly different. We next examined the antioxidant defense systems of these cells to determine whether cadmium exposure inhibited the cell’s normal antioxidant activity and thereby induces transcriptional change. Two different assays were performed to evaluate the effects of chronic cadmium exposure on ROS (reactive oxidative species) neutralization. Cadmium is a known disruptor of glutathione (GSH), binding directly to GSH and preventing it from neutralizing reactive oxygen and nitrogen species. Additionally, superoxide dismutase (SOD) activity was measured since it is known to aid in the cellular antioxidant defense mechanism. We hypothesized that GSH levels and SOD activity would decrease as a result of chronic cadmium exposure. These results will demonstrate whether cadmium-induced oxidative stress could occur through inadequate ROS neutralization.