Browsing by Author "Anderson, Jordan"
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Item The Effects of 17α-Ethinylestradiol (EE2) and Hydroxypropyl-β-Cyclodextrin (HPβCD) on the heart rate and metabolism of Embryonic Japanese Medaka (Oryzias latipes)(2019-04-01) Anderson, Jordan; Holdway, DouglasEstrogen toxicity has been an area of priority in aquatic toxicology over the last 20 years. The toxicity of a known estrogen mimic, 17α-ethinylestradiol (EE2), has been attributed to classical estrogen signaling within target and non-target organisms. Recent evidence has indicated that a rapid, non-genomic, non-classical estrogen signaling pathway also exists via the G protein coupled estrogen receptor (GPER). GPER is expressed ubiquitously and has many biological functions, including cardiovascular and metabolic function. Understanding the role of GPER at environmentally relevant concentrations of estrogens could aid addressing many knowledge gaps associated with estrogen toxicity in aquatic environments. This thesis investigated the effects of EE2 on heart rate and metabolism, as well as EE2 uptake, and elimination in embryonic Japanese medaka (Oryzias latipes). Bradycardia (reduced heart rate) was observed in embryos exposed to 10 ng/L of EE2. It was demonstrated that these effects were the result of GPER activation and not estrogen receptor (ER) α and β. A mixture of EE2 and hydroxypropyl-β-cyclodextrin (HPβCD) was also investigated. HPβCD is a commonly used odour suppressant and excipient with the ability to include guest compounds. It was determined that the observed EE2 induced bradycardia was reduced with a 4:1 HPβCD : EE2 molar ratio. Uptake of 14C-EE2 followed a sigmoidal pattern, and chorion permeability increased as development progressed. Elimination of 14C-EE2, showed a pattern of exponential decay following exposure from 6-48 hours post fertilization. HPβCD did not impede uptake of 14C-EE2 across the chorion, suggesting that HPβCD may cross the chorion. Uptake of the HPβCD – EE2 mixture into the tissues of the developing embryo should be investigated. A conclusive link was not determined between EE2 induced bradycardia and embryonic oxygen consumption (metabolic rate). The absence of metabolic effects might be mitigated by cutaneous gas exchange by embryonic fish. This data suggests that embryonic heart rate may not be an ideal measure of metabolic rate in embryonic medaka. This thesis is valuable to the field of aquatic toxicology as it highlights GPER as a novel mechanism of action for EE2 toxicity as well as the role of HPβCD in mixture toxicity. This work and future research into the role of GPER will aid in the overall understanding of estrogen toxicity to fish.Item The effects of Hydroxypropyl-β-Cyclodextrin on the American Flagfish (Jordanella floridae) over one complete life-cycle(2013-08-01) Anderson, Jordan; Holdway, DouglasUnderstanding the impacts of pharmaceuticals and personal care products (PPCPs) on aquatic ecosystems is an important issue in aquatic toxicology. Many PPCPs have been shown to cause effects on aquatic biota within detected environmental ranges. One compound of particular interest is hydroxylpropyl-β-cyclodextrin (HPβCD), the active ingredient in Febreeze®, and widely used for many applications. HPβCD is amphiphilic, toroidal in shape, and able to form non-covalent inclusion complexes with a variety of guest molecules. HPβCD has been shown to reduce volatility as well as improve the aqueous solubility of apolar guest compounds. As such, the use of HPβCD in the pharmaceutical and personal care industry has dramatically increased. With increasing potential for entering the environment through wastewater treatment plant (WWTP) effluent, HPβCD poses an unknown risk to non-target aquatic biota. As a result, a 145-day chronic full life-cycle exposure using American flagfish (Jordanella floridae) was completed using flow-through concentrations of 0 (control), 5, 16, 50,160, 500, and 1600 μg/L of HPβCD maintained via a peristaltic pump. No significant differences were observed in growth, condition factor (K) and hepatosomatic index (HSI) when chronically exposed to HPβCD (P ≤ 0.05). A significant increase in female gonadosomatic index (GSI) occurred in those exposed to HPβCD (P ≤ 0.05). A reduction in the time to reach steady-state spawning occurred at 1600 μg/L of HPβCD, while an increase in the total number of days eggs were laid was observed at 16, 160, and 1600 μg/L of HPβCD (P ≤ 0.05). A temporary reduction in offspring total length occurred at 21 days post hatch at 5, 16, 50, 160, and 500 μg/L of HPβCD (P ≤ 0.05). Finally, larval offspring from parents exposed to HPβCD showed a moderate 3-fold decrease in tolerance to acute copper toxicity.