This thesis has explored the nature of cellular behaviour in response to the mobility of ligands presented on supported lipid bilayers of varying viscosity (diffusive characteristics). This was inspired by the various characteristics of the in vivo microenvironment, controlling the cell response. For example, the viscoelastic, topographical, or chemical nature of the extracellular matrix can control cellular behaviours, such as adhesion, proliferation, migration and differentiation. Numerous biomaterials have alternately sought to understand the nature of the cell response and also to take advantage of it; the current work predominantly falls into the former of these categories. Whereas elastic stiffness is one side of the coin of viscoelasticity, viscosity is the other. Further, while much work has sought to understand the nature of both the elastic and viscoelastic nature of the cell response, as of yet few have sought to understand the role of viscosity in isolation. This is despite some work seeking to take advantage of this viscosity, by observing cellular behaviour on surfaces with known viscous components. This work has noted that cellular adhesion and spreading, focal adhesions, and differentiation are all affected by the viscous component of the surface without addressing why. Supported lipid bilayers (SLBs) present an excellent opportunity to understand these mechanisms. Commonly used as biosensing platforms, non-fouling coatings and model systems, they have also found use in both cell culture systems and in understanding mechanobiology. Individual lipids may exhibit a phase transition, Tm, at a temperature defined by the chemistry of the SLB component lipids; as such, they can exhibit significantly different, viscosity-defining, diffusive characteristics. This work describes the use of SLBs of differing Tm¬ that exhibit fluid-like or gel-like properties in cell culture conditions. These non-fouling SLBs were functionalised with the cell adhesive ligand RGD, derived from the matrix protein fibronectin, with the response of the cell on both the cell-wide and molecular scale determined. The cell response was then understood via pathways related to the mechanical sensing of the environment. Further, initial forays into the nature of the response of human mesenchymal stem cells (hMSCs) was determined, to test the applicability of the system to the overall field of biomedical engineering.

The activities of competing wood decay fungi bring about the decomposition of deadwood. The rate of decomposition is determined by the community composition, which is shaped by competitive interactions. Fungi compete with one another for territory and resources within 3 dimensional space via the production of an arsenal of inhibitory chemical compounds, yet interspecific interactions and chemical warfare within communities have never before been studied in 3 dimensional resources. This thesis, therefore, aims to determine how interactions cause metabolic processes to change, and, by the use of novel 3 dimensional systems, how those processes are affected by increased species diversity and spatial heterogeneity. Overarching hypotheses which have driven investigations are: (1) secondary metabolism and interaction outcome are inherently linked, both of which are affected by environmental conditions, (2) changes to spatial distributions and increased species diversity cause interaction outcomes and community dynamics to alter, and (3) changes to metabolic strategies for antagonism and resource utilisation will reflect alterations to community dynamics. Transitive interactions in pair wise 2 dimensional systems often became intransitive in species richer 3 dimensional systems, and the extent of patch fragmentation determined the length of coexistence of individuals within communities. Production of secondary metabolites comprising the fungal chemical weaponry, namely extracellular lignocellulolytic enzymes and volatile organic compounds (VOCs), was significantly different between 2 and 3 dimensional systems, between systems of varied species diversity, and between different spatial distributions of fungi, reflecting the observed changes to community dynamics. Furthermore, the production of intracellular metabolites which function in the biosynthesis pathways of antimicrobial compounds and agents of decay, was affected by species diversity, spatial distributions and territory fragmentation. Additionally, secondary metabolism and interaction outcome were found to be inherently linked, and affected by abiotic conditions. Specifically, interaction outcomes changed under different temperatures, and when wood was pre colonised for different lengths of time. Changes to the production of both enzymes and VOCs reflected the different outcomes, as either the cause or effect of outcome changes. These conclusions not only confirm the thesis hypotheses, but also demonstrate the importance of environmental conditions, species diversity and spatial dynamics to fungal community dynamics and forest ecosystem functioning.

Mesenchymal stem cells (MSC) are multipotent stem cells that have much potential for application in regenerative medicine, with their ability to self-renew and to undergo differentiation into several lineages, including those that comprise fat, bone, and cartilage. Studies on MSCs have mainly focused on exploiting their capacity to differentiate, rather than self-renewal, yet understanding of the latter process is pivotal for the expansion of these cells to sufficient numbers for use in future clinical treatments. Aspects of MSC behaviour can be induced by culture on nanopatterned substrates, known as nanotopography. Use of established nanopit features, in arrangements known to maintain MSC multipotency over long periods in culture (SQ), in addition to an osteogenic promoting arrangement (NSQ), were used as a tool to study self-renewal in MSCs, and begin to elucidate some of the potential mechanisms underlying the effects of the nanotopographies on stem cell fate. This study utilised patient-specific primary MSCs derived from bone marrow, which were optimised in terms of initial seeding density, to make efficient use of our nanotopographies. Once the fundamental details pertaining to optimal conditions for use of the substrates and cells were established, exploration of changes in metabolism, cell cycle and gene expression were carried out. Results indicated that MSCs on SQ contained more unsaturated metabolites, and that cell cycle may be altered, which warranted further investigation. Further study identified some differences in cell cycle regulatory proteins when compared to NSQ and flat controls. Further inferences were achieved by analysis of transcript abundances and differential expression, supporting the hypothesis of a heterogeneous population existing on NSQ, and activation of pathways linked to differentiation, consistent with previous work. A greater percentage of MSCs on SQ were shown to be in the early G0/G1 stages of the cell cycle in comparison to those on flat, suggesting that cell cycle is altered and further establishes a link between self-renewal and cell cycle regulation. Nanotopography was assessed for a novel application, namely the potential of SQ to reprogram differentiating MSCs. Nanotopography was used to induce and reverse the onset of osteogenic differentiation, and evaluated in conjunction with the addition of an epigenetic modifier, valproic acid. Results did not indicate that nanotopographical cues were able to reprogram MSCs. However, promising indications that stem cell marker STRO-1 levels increased, is consistent with SQ being a surface that maintains ‘stemness’ and multipotency of MSCs with culture in vitro.

Marine ecosystems are facing a diverse range of threats, including climate change, prompting international efforts to safeguard marine biodiversity through the use of spatial management measures. Marine Protected Areas (MPAs) have been implemented as a conservation tool throughout the world, but their usefulness and effectiveness is strongly related to climate change. However, few MPA programmes have directly considered climate change in the design, management or monitoring of an MPA network. Under international obligations, EU, UK and national targets, Scotland has developed an MPA network that aims to protect marine biodiversity and contribute to the vision of a clean, healthy and productive marine environment. This is the first study to critically analyse the Scottish MPA process and highlight areas which may be improved upon in further iterations of the network in the context of climate change. Initially, a critical review of the Scottish MPA process considered how ecological principles for MPA network design were incorporated into the process, how stakeholder perceptions were considered and crucially what consideration was given to the influence of climate change on the eventual effectiveness of the network. The results indicated that to make a meaningful contribution to marine biodiversity protection for Europe the Scottish MPA network should: i) fully adopt best practice ecological principles ii) ensure effective protection and iii) explicitly consider climate change in the management, monitoring and future iterations of the network. However, this review also highlighted the difficulties of incorporating considerations of climate change into an already complex process. A series of international case studies from British Columbia, Canada; central California, USA; the Great Barrier Reef, Australia and the Hauraki Gulf, New Zealand, were then conducted to investigate perceptions of how climate change has been considered in the design, implementation, management and monitoring of MPAs. The key lessons from this study included: i) strictly protected marine reserves are considered essential for climate change resilience and will be necessary as scientific reference sites to understand climate change effects ii) adaptive management of MPA networks is important but hard to implement iii) strictly protected reserves managed as ecosystems are the best option for an uncertain future. This work provides new insights into the policy and practical challenges MPA managers face under climate change scenarios. Based on the Scottish and international studies, the need to facilitate clear communication between academics, policy makers and stakeholders was recognised in order to progress MPA policy delivery and to ensure decisions were jointly formed and acceptable. A Delphi technique was used to develop a series of recommendations for considering climate change in Scotland’s MPA process. The Delphi participant panel was selected for their knowledge of the Scottish MPA process and included stakeholders, policy makers and academics with expertise in MPA research. The results from the first round of the Delphi technique suggested that differing views of success would likely influence opinions regarding required management of MPAs, and in turn, the data requirements to support management action decisions. The second round of the Delphi technique explored this further and indicated that there was a fundamental dichotomy in panellists’ views of a successful MPA network depending upon whether they believed the MPAs should be strictly protected or allow for sustainable use. A third, focus group round of the Delphi Technique developed a feature-based management scenario matrix to aid in deciding upon management actions in light of changes occurring in the MPA network. This thesis highlights that if the Scottish MPA network is to fulfil objectives of conservation and restoration, the implications of climate change for the design, management and monitoring of the network must be considered. In particular, there needs to be a greater focus on: i) incorporating ecological principles that directly address climate change ii) effective protection that builds resilience of the marine and linked social environment iii) developing a focused, strong and adaptable monitoring framework iv) ensuring mechanisms for adaptive management.

Pectin was isolated by aqueous extraction at pH 6.0 or 2.0 from okra (Abelmoschus esculentus L.) pods. An isolation protocol was designed to extract pectin and study the influence of the extraction pH on its chemical composition, macromolecular and functional properties. The extraction protocols resulted in the isolation of pectin of high purity as evidenced by their high total carbohydrate (70.0 – 82%) and low protein (4.3 – 6.3%) contents. Samples contained between 47-57% galacturonic acid, had broad molecular weight distributions, a low degree of methylation (40 and 25 %) and high degree of acetylation (52 and 38 %). Neutral sugar analysis showed that pectin extracted at pH 6.0 contained more neutral sugars, particularly, galactose, rhamnose and arabinose than that extracted at pH 2.0 indicating variations in fine structure. In addition, molecular parameters of the isolated pectins, such as intrinsic viscosity (2.8 – 4.4 dL g-1), critical concentration (0.15 – 0.45 dL g-1) and coil overlap parameter (0.66 –1.51), showed that extraction conditions resulted in pectin with different chain macromolecular characteristics. Following extraction, the functional properties of okra pectin were investigated in high and low moisture systems and also in colloidal dispersions. It has been shown that okra polysaccharides are non-gelling pectins and their inability to form ordered structures was attributed to the high degree of acetylation and branching of the side-chains. The pH sensitivity of okra pectins has been further demonstrated in high solid systems, where the mechanical relaxation of LM-pectin in the presence of co-solute has been altered by pH. It has been shown that high pH values result in extended chain conformation and early vitrification events. In contrast, viscoelastic functions of polyelectrolyte decreased and resulted in delayed vitrification events at low pH. The next step of present work was focused on potential utilization of okra polysaccharides in fabrication of oil-in-water emulsions for food and pharmaceutical applications. The emulsifying properties of crude okra extracts and okra isolates (rich in pectin) have been investigated under different conditions (e.g., oil volume fraction, biopolymer concentration, pH values, energy input methods) in order to produce fine emulsions with long-term stability. It has been shown that pH of extraction has a pronounced effect on the interfacial activity of both crude extract and pectin isolates. Extracts or isolates obtained at high pH demonstrated higher emulsifying capacity than those extracted at low pH. In general, okra pectin isolates were more efficient in emulsion stabilisation than crude extracts by producing emulsions of smaller droplet sizes. Moreover, emulsifying capacity of okra pectin was affected by the pH and stable emulsions were produced only at low pH values (pH 2.0 or 3.0). It has been shown that okra pectin-stabilized emulsions evolve under the effects of Ostwald ripening and coalescence during the long-term storage. The present work shows the potential of okra pectins as emulsifiers under acidic conditions and serves as the basis for the development of such systems in encapsulation technology of bioactive components.

Melanoma is notoriously resistant to immuno- and even targeted chemotherapeutic strategies despite recent advances in drug development. The overall mortality of melanoma correlates with its ability to metastasise. Breslow thickness or the depth of invasion remains the most useful prognostic indicator, thereby linking the ability of the cells to invade with their propensity to metastasise. Invasion occurs early during tumour development, but the factors driving this process remain poorly understood. There is a growing appreciation that chemotaxis plays an important role in driving the migration and invasion of melanoma cells, but the key stimuli are not known. Through the generation and validation of an improved chamber for cancer cell chemotaxis, melanoma cells are shown to create chemotactic gradients that drive or disperse themselves outwards with remarkable efficiency. This process is driven by strikingly positive chemotaxis and depends on the melanoma reaching a critical density to generate the gradient. The principal attractant is the inflammatory signal lysophosphatidic acid (LPA). Unexpectedly, it is active across all stages of melanoma evolution and LPA is both necessary and sufficient for chemotaxis in 2D & 3D assays. Growth Factors were previously considered to play essential roles in driving directed migration, but instead facilitate LPA chemotaxis. Sampling across the margins of melanomas in vivo, gradients of LPA are reliably identified, which are capable of driving accurate chemotaxis. This not only confirms the physiological importance of the results, but also is the first time a chemoattractant gradient has been measured in vivo. The corollary of these findings is that, provided with an external homogenous source of LPA, a large enough melanoma will degrade the local LPA to generate an outward gradient. Therefore it is the ability to degrade the gradient that acts as the signal to drive chemotaxis and invasion rather than the presence of LPA per se. In the chambers, cells are observed dispersing in a wave and in addition to driving efficient melanoma invasion, this may be responsible for the patterning of melanocytes across the skin during embryogenesis. Ultimately, identifying key aspects of and targeting the LPA-axis may prove a novel prognostic indicator and therapeutic target for invasion and metastasis.

Theileria annulata is an intracellular, tick-transmitted apicomplexan parasite, which causes tropical theileriosis in cattle. It undergoes a complex life cycle with several distinct stages occurring within the bovine host and tick vector. ApiAP2 proteins are key candidate transcription factors for regulation of stage specific gene expression across apicomplexans. They are differentially expressed in specific developmental stages and certain ApiAP2s bind specifically to unique DNA sequence motifs. Identification of stage-specific expression of putative transcriptional regulators, the motifs they bind to and potential target genes provided the rationale for this study to understand the molecular mechanisms that control stage differentiation to the merozoite in T. annulata. The results demonstrated that T. annulata ApiAP2s show marked differences in expression levels during the parasite life cycle. ApiAP2 target DNA motifs orthologous to those in Plasmodium and Cryptosporidium were also discovered in Theileria intergenic regions, indicating that the genes downstream are potential targets of Theileria ApiAP2s. These motifs were also found in upstream regions of up-regulated TaApiAP2 genes, suggesting possible auto-regulation and an interaction network of ApiAP2 transcription factors. Importantly ApiAP2 fusion proteins up-regulated during differentiation to the merozoite stage bound to their predicted specific DNA motifs validating that ApiAP2 DNA-binding domain structure is conserved across Apicomplexa genera. Evidence was also produced that AP2 proteins play important roles in steps that commit a cell to differentiate: TA13515D is the orthologue of the AP2G factor in Plasmodium that is a major regulator of gametocytogenesis: TA16485 may be involved in down-regulation of genes during merogony and expression of TA11145 at a higher level in a cell line competent for merogony relative to a line severelly attenuated indicated involvement in regulation of this differentiation step. Discovery of multiple nuclear factors binding to a 2x(A)CACAC(A) motif implicated in autoregulation of TA11145, together with phylogenetic evidence for a clade of related domains that bind this motif suggest that multiple competing ApiAP2s may operate to regulate stochastic commitment to merozoiteproduction. Based on this data an updated stage differentiation model has been generated, with up regulation of the TA11145 gene a key event. A C-box motif association with genes implicated in establishment of the transformed host cell (TashAT, SVSP) suggests it could be important for deregulation of this event as the parasite undergoes stage differentiation. In contrast the inverse G-box was found associated with genes up-regulated from merozoite to piroplasm. EMSA analysis of parasite nuclear extract with a G/Cbox motif probe showed that the motif is an active binding site for a stage regulated nuclear factor. Specific binding of candidate TA12015 protein to the G/C-box motif was unable to be confirmed. Taken together, these results provided evidence that ApiAP2 proteins are regulators of stage-specific gene expression in T.annulata. They also provide insight into probable ApiAP2 interaction networks and support the postulation of a differentiation mechanism conserved across the Apicomplexa. Finally, the data suggests that this mechanism is stochastic and is likely to occur via a positive feedback loop generating a threshold that commits the cell to differentiate to the next stage of the life cycle.

Neuroblastoma is the most common solid extracranial tumour in children. The neuroblastoma SH-SY5Y cell line is a third successive subclone established from a metastatic bone tumour biopsy. It can be induced to differentiate (regress) into a neuronal phenotype when treated with any of several molecules including retinoic acid (RA). This characteristic has been exploited in several studies that use the SH-SY5Y cell line as a neuronal model. These studies have had far- reaching implications in shaping our understanding of certain key aspects of neurotoxicity and neurodevelopment yet their genuine relevance becomes evident when approached from an oncological point of view, as they provide information about the process underlying tumour regression which in turn can lead to the development of better therapies for the clinical management of this malignancy. It has been shown both in vitro and in vivo that several tumours constitutively catabolize the essential amino acid tryptophan (Trp) promoting cancer- associated inflammation, immune response suppression, immune escape and tumour outgrowth. The main degradation pathway of Trp is the kynurenine pathway: it involves its transformation into several bioactive compounds such as kynurenic acid (KA) and quinolinic acid (QA). QA has been implicated in several neurodegenerative diseases where it is believed to induce excitotoxic neuronal death through the activation of the N-methyl-D-aspartate (NMDA) receptor, a type of ionotropic glutamate receptor, as well as by causing oxidative stress and energy metabolism disruption. Conversely, KA acts as an NMDA receptor antagonist and exerts neuroprotection. Similarly, glutamate signaling and its dysregulation has been implicated in the development and progression of cancer. Furthermore, several glutamate receptor antagonists, including kynurenic acid, have been shown to inhibit the proliferation and migration of neoplastic cells. Conversely, it has recently been reported that QA increases the proliferation of SK-N-SH cells and protects gliomas against oxidative stress by acting as a precursor of NAD+. In view of all that has been mentioned thus far, the SH-SY5Y cell line was used as a model to investigate the effect of certain Trp metabolites such as QA, KAand 3-hydroxyanthranilic acid (3-HAA) on cellular morphology, viability and neurite extension. An important part of this study was to determine whether the available methods could reliably be employed to investigate these parameters in the SH-SY5Y cell line. It was confirmed that the acquired SH-SY5Y cell line retains its ability to differentiate and to die, and that both processes can be accurately quantified. Additionally, the optimal culturing conditions for the SH- SY5Y cell line were determined. Treatment with RA (10 μM) was used as a positive control of differentiated SH- SY5Y cells. Overall, the morphology adopted by cells after QA (50 μM) treatment was similar to the one that follows RA-induced differentiation. It was demonstrated that QA caused an increase in the neurite/soma ratio in SH-SY5Y cells, which was confirmed by Western blot analysis as evidenced by an increase in the total cellular content of β3-tubulin. These results were also confirmed by a neurite outgrowth assay that selectively quantified the neuritic mass present in cultures. However, unlike RA, QA did not decrease the levels of the neuronal proliferation marker doublecortin; the term neuritogenesis is therefore more appropriately used to refer to the series of morphological and molecular changes induced by QA in SH-SY5Y cells. The morphological changes induced by QA were not reproduced by application of NMDA, nor were they inhibited by blockade of the NMDA receptor with MK-801. Furthermore, SH-SY5Y cells were not susceptible to NMDA excitotoxic death. In view of this, the expression of GluN1 protein was determined by Western blot. GluN1 could not be detected in either undifferentiated or differentiated SH-SY5Y cells, confirming that QA-induced neuritogenesis occurs through a mechanism independent of NMDAR activation. The results herein contained suggest that the SH-SY5Y cell line does not have functional NMDARs, nonetheless it is recognized that a more exhaustive study would be necessary to fully establish which glutamate receptor subtypes are found in the SH-SY5Y cell line. The effect of QA on the production of reactive oxygen species (ROS) was also investigated. QA caused an increase in the intracellular levels of ROS as evidenced by an increase in the fluorescence of oxidised ethidium. Additionally QA-treatment caused an increase in the expression of NRF2, a transcriptionfactor that responds to oxidative stress and which has been implicated in ROS- induced differentiation in SH-SY5Y cells. In contrast, superoxide dismutase (SOD; 300 U/ml) significantly reduced the levels of ROS induced by QA treatment, which in turn caused an increase in cell proliferation and a reduction in the number of neurites. Similarly, diphenylene iodonium (DPI; an inhibitor of NADPH oxidase) also inhibited QA-induced neuritogenesis. These results suggest that the action mechanism of QA is mainly via the production of ROS, most likely superoxide (O2•-) through NADPH-oxidase. Interestingly, nicotinamide (1 nM-1mM; another precursor of NAD+) caused a dose dependent increase in the number of neurites and in the expression of β3- tubulin, which suggests that the action mechanism of QA may be mediated by metabolites of the nicotinate and Nam pathway, including NAD+ either before or after the induction of ROS. Cells were treated with 3-hydroxyanthranilic acid (3-HAA) in order to ascertain whether other pro-oxidant molecules could induce neuritogenesis as well. Single and repeated application of 3-HAA (100 μM) induced cell death in SH-SY5Y cells. Furthermore, when 3-HAA was delivered in combination with SOD, there was a shift in the IC50 values indicating that toxicity was potentiated by SOD. Catalase (CAT; 100 U/ml) afforded complete protection from the exacerbated damage induced by the single co-application of 3-HAA + SOD. However, when repeated treatments were performed, CAT no longer afforded any protection. Interestingly, the serum concentration in the medium did not affect the IC50 of 3-HAA but it did modulate the response to CAT, indicating that the specific ROS produced after 3-HAA treatment depend on the medium in which 3-HAA is delivered. At sublethal doses, 3-HAA interfered with the expression of NeuN (neuronal marker) through a mechanism that involves high production of ROS. The ability of some kynurenines to induce differentiation and cell death in SH- SY5Y cells may open new and exciting avenues of research. If these results can be confirmed in vivo they could impact the way in which certain neuroblastomas are treated.

With a globally ageing population diseases associated with this natural process are becoming major issues worldwide. Research into the process of ageing and its concomitant issues is rapidly expanding; the need for new tools and models to investigate this rapidly expanding arena of research is paramount. The discovery of a spontaneous mutation in the AS rat strain which introduces a premature stop mutation into the gene encoding protein kinase C γ (PKCγ) lead to the development of a model for one such age related disorder, Parkinson's disease. Consequently, this model has been selected to investigate age related changes in specific areas of the brain (the cerebellum, basal ganglia, cerebral cortex and brainstem). These regions were selected because they have previously been shown to demonstrate changes with age (cerebellum, cerebral cortex and basal Ganglia), they show differences between the AS and AS/AGU strains (basal ganglia) or they show differences in PKCγ knockout models (cerebellum). The Brainstem was selected as it shows little change due to age and shows no differences in PKCγ knockouts or AS/AGU rats. This study used established qPCR methods to measure a validated biomarker of ageing, CDKN2A (the transcript for p16^INK4a) in the brains of these rats to determine whether this model is in fact a genuine model for accelerated ageing. This thesis demonstrates that CDKN2A expression, in combination with senescence-associated β-galactosidase staining, provides clear evidence of accelerated ageing in the brains of AS/AGU rats when compared with the parent AS strain. These investigations were furthered by an investigation of members of the Sirtuin family of proteins. The changes in expression of these Sirtuins indicates that there may be increased levels of cellular stress, disruption of metabolism and DNA damage in the AS/AGU rats, this would be congruent with the accelerated ageing phenotype present in this strain. Furthermore, the levels of these Sirtuins were in line with the predictions from the MTR trinity in regards to the accelerated ageing phenotype. Whilst some of the changes in senescence and metabolic disruption may be attributable to the PKCγ mutation in the AS/AGU rats, it would appear that there is some element of accelerated ageing that is independent of this mutation.

Microplastic pollution has been identified as an ever increasing proportion of marine litter. Despite an increase in microplastic awareness over the last decade, it represents an as yet unquantified threat to the marine environment. The relatively few studies that monitor its distribution and impact have illustrated a range of worrying effects on marine habitats and communities. The Clyde Sea Area (CSA) is subject to many sources of terrestrial and maritime plastic input. The use of plastics in recreational and commercial vessels throughout the CSA is believed to result in large levels of microplastic fibres, which have previously been seen to be ingested by a range of marine organisms. In a study of the breakdown of commonly used polymers in benthic environments, it was found that ropes of 10 mm diameter in sub-tidal conditions release between 0.086 and 0.422g of microfibers per meter per month in the early stages of degradation. This rate would be expected to increase over subsequent months, releasing substantial amounts of fibres into the CSA environment. In addition to the presence of numerous sources of microplastics, the CSA is relatively enclosed, and may accumulate high levels of debris as a result. Monthly sampling of the water and sediment in the CSA revealed contamination similar to that observed in other near-shore environments. Thus, it is expected that the potential threat to organisms in other areas will be similar to that observed in the CSA. One organism known to take up microplastics is the Norway lobster, Nephrops norvegicus, the target of the main fishery in the CSA. In this work we examined the levels of microplastic in the gut of N. norvegicus from the Scottish waters. Examination of individuals from the CSA revealed both a high occurrence and high accumulation of microplastic. This was found to be much greater than in N. norvegicus sampled from more remote Scottish waters. As a result, N. norvegicus from the CSA are most likely to suffer from the negative impacts associated with microplastic ingestion than those in offshore or in areas of low anthropogenic activity. In order to determine the potential impacts of microplastic ingestion on N. norvegicus, we first examined the mechanism by which N. norvegicus retain and egest microplastic. The position of microplastic aggregations in the foregut indicates that the gastric mill is the main obstacle to microplastic egestion. Inducing moult in microplastic-fed individuals demonstrated that expulsion of the gut lining during ecdysis enables N. norvegicus to reduce their plastic load, limiting plastic aggregation to the length of a single moult-cycle. In an 8 month controlled-feeding experiment retained plastic was seen to have a range of impacts on N. norvegicus. Feeding rate and body mass was seen to decrease in plastic loaded N. norvegicus, and a reduction was observed in a number of indicators of nutritional state. The results presented in this thesis have a number of implications to the CSA and wider marine environment. The similarity in the level of microplastic observed in the CSA to that of other studies of inshore waters indicates the potential for high microplastic uptake by crustaceans in those areas. The high variability in observed microplastic abundance suggests that small-scale monitoring is unsuitable for monitoring marine microplastic debris, and that use of an indicator species may provide a more reliable method of monitoring that is not subject to small-scale heterogeneity in distribution. The seasonal retention of microplastic by N. norvegicus indicates that crustaceans may provide a suitable indicator of local contamination. However, in the CSA, the high level of fibre aggregation and observed impacts of prolonged retention indicate that microplastic may be causing further pressure on an already exploited resource, reducing the stability of the valuable N. norvegicus population.