All sea turtle populations face the risk of extinction. Of the threats to sea turtles, the effects of environmental chemicals are the least understood. Polychlorinated biphenyls (PCBs) are toxic, persistent, ubiquitous, anthropogenic halogenated organic contaminants (HOCs). While anthropogenic HOCs are notorious for their toxicity, exposure to naturally produced HOCs, many of which exist in the marine environment, may also cause adverse effects. The purpose of this dissertation was to gain insight into possible impacts of HOCs on the health of sea turtle populations by assessing biotransformation enzymes, as well as the accumulation and metabolism of HOCs in several species of sea turtles- loggerhead (Caretta caretta), green (Chelonia mydas), olive ridley (Lepidochelys olivacea), and hawksbill (Eretmochelys imbricata).
The results showed that sea turtle livers possess the biotransformation enzymes cytochrome P450 (CYP) and glutathione S-transferase (GST). Western blots revealed CYP2- and CYP3-like proteins, but do not CYP1A-like proteins. Spectrophotometric assays indicated that sea turtles showed similar GST kinetic parameters, but inter- and intra-species variation in activities towards GST class-specific substrates. PCBs accumulated in the livers of sea turtles, with levels ranging from 5-25 ng/g, as measured by gas chromatography with electron capture detection. In vitro incubations of sea turtle liver microsomes with 2,2',5,5'-tetrachlorinated biphenyl (PCB 52) indicated the formation a hydroxylated metabolite by liquid chromatography/mass spectroscopy, while incubations with 3,3'4,4'-tetrachlorinated biphenyl (PCB 77) did not reveal metabolites. Taken together, these results supported a model in which rates of hepatic biotransformation may determine elimination and relative concentrations of PCBs in reptilian tissues.
Hawksbill sea turtles feed primarily on marine sponges, which produce natural HOCs, such as 4,5-dibromopyrrole-2-carboxylic acid (DBPC), as deterrents against predation. The lack of detectable in vitro metabolism of DBPC by hawksbill sea turtles, as measured by liquid chromatography with radioactivity detection, indicated that biotransformation may not be the primary mechanism of tolerance to natural dietary. Kinetic analysis of spectrophotmetric assays indicated non-substrate binding of DBPC by GST, which suggested potential protection from sponge HOCs via GST transport or sequestration. The information in this dissertation provides critical knowledge to connect toxic effects of HOCs to sea turtle population decline.