Honors College
 

Document Type

Honors Thesis

Publication Date

Spring 5-2016

Abstract

2,4-Dinitrophenol (DNP) is a well-documented mitochondrial uncoupler that was widely used as a dieting drug in the 1930’s. It was later banned in 1938 due its negative side effects which included extreme weight loss, the formation of cataracts, skin rashes, and death. Triclosan (TCS) is a common antimicrobial agent that is a component in soaps, toothpastes, and other household products. In addition to its antimicrobial role, TCS has been found to alleviate skin inflammation and dermatitis. However, TCS has also been linked to several health issues including increased cases of asthma and allergy, developmental problems, and decreased fertility. Previous studies in the Gosse laboratory found that TCS inhibits the primary functions of mast cells, key players in the immune system. More recent studies have found that in addition to increasing oxygen consumption, TCS significantly inhibits ATP production in rat basophilic leukemia cells, clone 2H3 (RBL-2H3) at non-cytotoxic doses with an EC50 of 7.5 µM to 9.6 µM. These results strongly indicate that, like DNP, TCS is a mitochondrial uncoupler.

Since DNP is a known, dangerous mitochondrial uncoupler, it serves as a useful comparison to assess the potential danger of TCS. In this study, cultured RBL-2H3 cells were exposed to increasing concentrations of DNP and were assessed for ATP production and cytotoxicity. DNP was found to significantly inhibit ATP production at non-cytotoxic doses with an EC50 of 389 µM to 677 µM. These results indicate that TCS is ~60-fold more potent as a mitochondrial uncoupler in RBL cells than in DNP. More related, comparative research with DNP is needed to fully explore triclosan’s mitochondrial toxicity.

Included in

Biochemistry Commons

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