The Prevention of Inflammatory-Related Liver Damage by Tamoxifen in Rats Given Fish Oil

Presenter Information

Renae Haycraft, Minnesota State University, Mankato

Location

CSU North Ballroom

Start Date

25-4-2006 10:00 AM

End Date

25-4-2006 12:00 PM

Student's Major

Biological Sciences

Student's College

Science, Engineering and Technology

Mentor's Name

Steven Mercurio

Mentor's Department

Biological Sciences

Mentor's College

Science, Engineering and Technology

Second Mentor's Name

Dana R. Quirk Dorr

Second Mentor's Department

Chemistry and Geology

Second Mentor's College

Science, Engineering and Technology

Description

The focus of this research was to decrease inflammatory-related liver damage from tamoxifen in rats by adding fish oil to the diet. Tamoxifen causes a significant increase in inflammation in the liver. Inflammation increases with the production of prostaglandins by a metabolic pathway involving arachidonic acid. Cytochrome P450, the enzyme that metabolizes tamoxifen, also causes an increase in the production of prostaglandins. The increased inflammation is related to lipid accumulation and ultimately lipid peroxidation in the liver. Resulting damage in humans includes hepatic steatosis (fatty liver), nonalcoholic steatohepatitis (NASH), and cirrhosis. Fish oils rich in omega-3 fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), should decrease inflammation by indirectly suppressing the production of prostaglandins. The metabolism of omega- 3 fatty acids competitively suppresses the metabolic pathway that produces arachidonic acid, therefore decreasing prostaglandin production. Success of the experiment was determined by giving female rats a 7-day treatment of tamoxifen concomitantly with dietary fish oils. The viability of the treatment was estimated by testing lipid accumulation, cytochrome P450 levels, lipid peroxidation, protein quantities and degree of cirrhosis.