Posted: Thursday, February 21, 2013
2013 Chemistry/Physics Seminar Series
Jaquan Williams, a master's degree candidate in the forensic science program, will present his master's thesis, "Comparative Metabolism of Phenanthro[3,4-b]thiophen and Its Carbon Analog Benzo[c]phenanthrene," at 12:30 p.m. today, February 21, in Science Building 272. This seminar series is sponsored by the Auxiliary Service Grant Allocation Committee, the Vice President for Student Affairs Office, and the Faculty-Student Association. The abstract is as follows:
Polycyclic aromatic hydrocarbons (PAHs) and their sulfur-heterocyclic PAHs (thia-PAHs) formed by incomplete combustion of organic matter are commonly occurring persistent environmental contaminants (1). A number of thia-PAHs have shown significant mutagenic and carcinogenic activities. As noted with PAHs, these chemical contaminants also require metabolic activation in order to exhibit their mutagenic and carcinogenic effects (2). In the present study, the metabolism of phenanthro[3,4-b]thiophene (P[3,4-b]T), a thiaster of weakly mutagenic benzo[c]phenanthrene (B[c]P), was investigated by liver microsomes from induced and un-induced rats as well as lung microsomes from smokers and nonsmokers. All the microsomes metabolized P[3,4-b]T to produce both ring oxidation products (predominantly P[3,4-b]T 8,9-diol) and S-oxidation products (predominantly P[3,4-b]T sulfone).
P[3,4-b]T is a more potent mutagen than its homocyclic analog B[c]P. Previous studies have shown that, like many carcinogenic PAHs, B[c]P is also metabolically activated to B[c]P 3,4-diol to produce mutagenic and carcinogenic effects (3). However, our recent studies with P[3,4-b]T, a sulfur analog of B[c]P, have shown that, in contrast to P[3,4-b]T 8,9-diol, a corresponding sulfur analog of B[c]P 3,4-diol, P[3,4-b]]T sulfone exhibit significantly higher mutagenic activity compared to P[3,4-b]T. This earlier finding, together with our present study that demonstrates the formation of P[3,4-b]T sufone as a metabolite of P[3,4-b]T, supports our hypothesis that, unlike B[c]P, P[3,4-b]T exhibits its mutagenic and possibly carcinogenic activity predominantly via sulfoxidation pathwa