EFFECTS OF DDT AND DDE ON IMMUNITY, OXIDATIVE STRESS AND REPRODUCTIVE PARAMETERS IN RODENTS
Type of DegreePhD Dissertation
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Lingering endocrine disrupting chemicals (i.e. DDT) are a significant threat to wildlife and humans. The effects of DDT have long been documented to cause adverse effects on reproduction, immunity and induce physiological changes. However, this type of ecotoxicological research predominantly focuses on the physiological changes caused by administering acute high dose ranges of these contaminants. There is a significant lack of research on the consequences of chronic exposure to environmentally relevant doses, although this exposure is the most experienced by and impactful to humans and wildlife in our current Anthropocene age. I tested 3 hypotheses in rodent species: (1) Peromyscus maniculatus and Sigmodon hispidus from the historically contaminated site would exhibit increased tissue contaminant load, decreased immune capability and a higher expression of oxidative stress biomarkers increasing probability of disease and decreased reproductive success; (2) early onset exposure of DDE will cause a greater inhibition of steroidogenesis and induce higher levels of oxidative stress in a dose-dependent manner during laboratory exposure; (3) that rats exposed chronically to environmentally relevant levels of DDE would exhibit decreased levels of testosterone and steroidogenic enzyme capacity (i.e. 3β HSD) in Leydig cells. We found that contaminant load was higher in Peromyscus maniculatus, the omnivorous species, than in Sigmodon hispidus, the predominantly herbivorous species, with each species showing an increase in a marker for oxidative stress. Additionally, both species exhibited a marked leukocytopenia which may indicate immune dysfunction. However, a traditional marker of exposure to stress (i.e., higher N/L ratio) did not differ significantly in either species when individuals from contaminated and reference areas were compared. Experimental DDE dosing in Long-Evans rats demonstrated a significant reduction in testosterone, with later onset rats being most affected contrary to our predictions. Moreover, we found an upregulation in a oxidative stress in a dose-dependent manner. Chronically dosed Long-Evans rats also showed a significant reduction of testosterone in Leydig cells which exhibited increased apoptosis and significant differences within the steroidogenic pathway. As a whole, this dissertation provides evidence that low levels of contaminants pose a threat in the environment with implications on immune responsiveness, cellular stress and especially steroidogenesis.