| dc.description.abstract | The oceans are changing, globally and locally. Two stressors already impacting marine life on both scales are changing carbonate chemistry, whether induced by the worldwide increases in atmospheric concentrations of carbon dioxide termed ocean acidification (OA) or by small-scale spatiotemporal fluctuations in coastal waters; and contamination, caused by the countless anthropogenically-produced chemicals that enter the marine environment each year. The potential for these two stressors to interact, causing novel toxicity outcomes for marine life, has only been acknowledged in recent years. In this thesis, I investigate interactions between carbonate chemistry alterations and contaminants to explore whether certain aspects of animal physiology and contaminant chemistry consistently determine outcomes for marine invertebrates.
Through a review of the state of knowledge on the biological impacts of these interactions, I highlighted key knowledge gaps. Whilst established models exist for the effect of freshwater pH on the toxicity of contaminants, this has rarely been investigated in a marine context. This was particularly significant for ionisable organic contaminants: in general, acidic compounds increase in toxicity within the OA-relevant pH range, whilst basic compounds decrease in toxicity. Additionally, there was strong potential for the fluctuations in carbonate chemistry which naturally occur in coastal habitats to alter the toxicity of pH-sensitive marine contaminants.
To address these knowledge gaps, I first exposed two marine invertebrates, the common mussel Mytilus edulis and the king ragworm Alitta virens, to the pH-sensitive contaminant copper under a fluctuating pCO2/pH regime representative of coastal conditions and which was expected to increase its toxicity. Fluctuating pCO2/pH induced an extracellular acidosis of 0.2 units for mussels, likely contributing to the twofold increases in oxidative stress and DNA damage induced by copper compared to in non-fluctuating conditions. For A. virens, its ability to maintain acid-base homeostasis in fluctuating conditions via accumulation of bicarbonate resulted in an extracellular alkalosis of 0.3 units. This mitigated copper toxicity which resulted in reduced DNA damage and oxidative stress compared to exposure to copper in non-fluctuating pCO2/pH conditions.
Secondly, I assessed reproductive parameters in early life stages of the painted urchin Lytechinus pictus and the lugworm Arenicola marina when exposed to two ionisable pharmaceuticals in OA conditions: tolcapone, which behaves as an acid and hence may increase in toxicity, and fluoxetine, which behaves as a base and hence may decrease in toxicity. In OA treatments both with and without pharmaceuticals, measurements of sperm swimming speed (curvilinear velocity, straight-line velocity and average path velocity) increased twofold for urchins, but decreased by half for lugworms, compared to ambient pH conditions. Pharmaceuticals altered the magnitude of the OA effects but not consistently: both pharmaceuticals decreased velocity measurements for lugworms in OA conditions, whilst tolcapone increased and fluoxetine decreased these effects for urchins. Additionally, these swimming parameters were differentially linked to fertilisation success for each species, resulting in differing outcomes which appeared to be driven predominantly by the physiology and reproductive ecology of each species in response to OA.
Finally, I exposed adult common mussels, Mytilus edulis, and purple urchins, Paracentrotus lividus, to these same pharmaceuticals in OA conditions, hypothesising that differences in species acid-base physiology would impact toxicity changes alongside the theorised ionisation changes. OA increased the effect of tolcapone on oxidative stress by 50 % in urchins, but not mussels. OA also increased the effect of fluoxetine on urchin antioxidant activity by 183 % and decreased ammonia excretion rate by 57 %; however, mussel antioxidant activity decreased by 73 % whilst oxygen uptake increased by 81 %. Importantly, the direction of OA-induced effects on these responses did not correspond to theorised changes to pharmaceutical ionisation, and the magnitude of effects did not correspond to differences in acid-base physiology.
Taken together, my findings demonstrate the importance of differences between species and life stages in determining their responses to the combination of altered carbonate chemistry and contaminants, and that the final toxicity outcomes for marine invertebrates cannot be estimated based solely on theorised chemical changes to contaminants in OA conditions. Whilst our knowledge of contaminants and changing carbonate chemistry as single stressors is increasing, marine organisms will experience both concurrently and this work contributes to our understanding of how these global and local stressors will interact in a future ocean. | en_GB |
