Date of Completion

Spring 5-1-2016

Thesis Advisor(s)

John B. Morris

Honors Major

Pharmacy Studies

Disciplines

Pharmacy and Pharmaceutical Sciences

Abstract

Through its toxic metabolites, acetaminophen can cause oxidative injury in the liver. This damage has not yet been investigated in the respiratory tract. If acetaminophen also causes oxidative stress and injury here, this widely used antipyretic could potentiate the adverse effects of oxidant air pollutants. Thus, the primary goal of this project is to determine if low non-hepatotoxic doses of APAP is correlated with an increase of oxidative stress in the airways, possibly linking APAP to the onset of asthma. Using data that reflected murine breathing patterns, the addition of acetaminophen greatly increased the reflex irritant response to ETS through the potentiation of the oxidant sensory irritant, most likely caused by acetaminophen’s metabolite, NAPQI.

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