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Item A Comparison of Hematological, Immunological, and Stress Responses to Capture and Transport in Wild White Rhinoceros Bulls (Ceratotherium simum simum) Supplemented With Azaperone or Midazolam(Frontiers Media S.A., 2020-10-20) Pohlin F; Hooijberg EH; Buss P; Huber N; Viljoen FP; Blackhurst D; Meyer LCR; Torrey SCapture and transport are essential procedures for the management and conservation of southern white rhinoceroses (Ceratotherium simum simum), but are associated with stress-induced morbidity and mortality. To improve conservation efforts, it is crucial to understand the pathophysiology of rhinoceros stress responses and investigate drug combinations that could reduce these responses. In this study we measured rhinoceros stress responses to capture and transport by quantifying hematological and immunological changes together with adrenal hormone concentrations. We investigated whether the potent anxiolytic drug midazolam was able to mitigate these responses compared to azaperone, which is more commonly used during rhinoceros transport. Twenty three wild white rhinoceros bulls were transported for 6 h (280 km) within the Kruger National Park for reasons unrelated to this study. Rhinoceroses were immobilized with either etorphine-azaperone (group A, n = 11) or etorphine-midazolam (group M, n = 12) intramuscularly by darting from a helicopter. Azaperone (group A) or midazolam (group M) were re-administered intramuscularly every 2 h during transport. Serial blood samples were collected at capture (TC), the start of transport (T0) and after 6 h of transport (T6). Changes in hematological and immunological variables over time and between groups were compared using general mixed models. Increases in plasma epinephrine and serum cortisol concentrations indicated that rhinoceroses mounted a stress response to capture and transport. Packed cell volume decreased from TC to T6 indicating that stress hemoconcentration occurred at TC. Neutrophils progressively increased and lymphocytes and eosinophils progressively decreased from T0 to T6, resulting in an increase in neutrophil to lymphocyte ratio; a characteristic leukocyte response to circulating glucocorticoids. A reduction in serum iron concentrations may suggest the mounting of an acute phase response. Rhinoceroses experienced a decrease in unsaturated fatty acids and an increase in lipid peroxidation products at capture and toward the end of transport indicating oxidative stress. Midazolam, at the dose used in this study, was not able to mitigate adrenal responses to stress and appeared to directly influence leukocyte responses.Item Effect of a pre-calving injectable trace mineral supplement on white blood cell function in seasonally calving pastoral dairy cows.(Taylor and Francis Group, 2024-10-30) Bates AJ; Wells M; Fitzpatrick C; Laven RAAims To investigate the effect of injection of trace mineral supplement (TMS) 14–28 days before calving on white blood cell count (WBCC) and function, serum antioxidant capacity (SAC) and reactive oxygen species (ROS) in pasture-fed cattle after calving. Methods On each of two South Island, seasonally calving, pastoral dairy farms,1 month before dry-off, a random sample of 150 multiparous cows predicted to calve within 7 days of the herd’s planned start of calving (PSC) were stratified on individual somatic cell count, age, breed and expected calving date. On each farm, 14–24 days before PSC, 60 selected cows were randomly assigned for TMS (Zn, Mn, Se, Cu) injection, and 60 were controls. All 240 cows were contemporaneously injected with hydroxocobalamin, and controls with Se. Blood samples were collected pre-injection and 3, 12 and 40 days after calving. Phagocytic activity, count and proportion of neutrophils, lymphocytes and monocytes, WBCC, ROS, SAC were measured. Plasma concentrations of Se, Cu and glutathione peroxidase (GPx) were monitored from a random subset of animals. Differences attributable to TMS were estimated using mixed-multivariable Bayesian analysis, expressed as mean and highest density interval (HDI). Results Three and 40 days after calving, TMS-treated cows had 0.36 (90% HDI = 0.00–0.77) x 109 and 0.25 (90% HDI = 0.00–0.55) x 109 fewer neutrophils/L. Neutrophils comprised 6 (90% HDI = 0–11)% and 4 (90% HDI = 0–8)% less of the WBCC, and the neutrophil count was 14 (90% HDI = 0–27)% and 9 (90% HDI = 0–18)% less than controls. However, 3 days after calving, there were 7 (95% HDI = 2–12)% more cells phagocytosing and 2,900 (95% HDI = 2,600–3,200) more bacteria ingested/cell. Twelve and 40 days after calving, TMS-treated cows had 0.65 (95% HDI = 0.17–1.17) x 109 and 0.28 (95% HDI = 0.00–0.59) x 109 more lymphocytes/L. Lymphocytes comprised 10 (95% HDI = 3–18)% and 5 (95% HDI = 0–9)% more of the WBCC, and the lymphocyte count was 30 (95% HDI = 11–51)% and 9 (95% HDI = 0–9)% more than controls. There were no meaningful differences in ROS, SAC, ROS/SAC, other white blood cells, or WBCC. Plasma Cu, Se and GPx concentrations were above recommended thresholds. Conclusions Pre-calving TMS injection was associated with differences in white blood cell population and function that may reduce the risk of disease. Abbreviations BHOB: Beta-hydroxybutyrate; GPx: Glutathione peroxidase; HDI: Highest density interval; MESF: Molecules of equivalent soluble fluorophore; OSi: Oxidative stress index; PSC: Planned start of calving; ROPE: Region of probable equivalence; ROS: Reactive oxygen species; SAC: Serum antioxidant capacity; THI: Temperature humidity index; TMS: Trace mineral supplement; WAIC: Widely applicable information criterion; WBCC: White blood cell count.Item The Role of Lifestyle and Dietary Factors in the Development of Premature Ovarian Insufficiency(MDPI (Basel, Switzerland), 2023-08-11) Shelling AN; Ahmed Nasef N; Dimitriadis, F; Sofikitis N; Sulyok EPremature ovarian insufficiency (POI) is a condition that arises from dysfunction or early depletion of the ovarian follicle pool accompanied by an earlier-than-normal loss of fertility in young women. Oxidative stress has been suggested as an important factor in the decline of fertility in women and POI. In this review, we discuss the mechanisms of oxidative stress implicated in ovarian ageing and dysfunction in relation to POI, in particular mitochondrial dysfunction, apoptosis and inflammation. Genetic defects, autoimmunity and chemotherapy, are some of the reviewed hallmarks of POI that can lead to increased oxidative stress. Additionally, we highlight lifestyle factors, including diet, low energy availability and BMI, that can increase the risk of POI. The final section of this review discusses dietary factors associated with POI, including consumption of oily fish, mitochondria nutrient therapy, melatonin, dairy and vitamins that can be targeted as potential interventions, especially for at-risk women and in combination with personalised nutrition. Understanding the impact of lifestyle and its implications for POI and oxidative stress holds great promise in reducing the burden of this condition.Item Hepatotoxicity of titanium dioxide nanoparticles.(John Wiley & Sons Ltd, 2024-05-13) Khan J; Kim ND; Bromhead C; Truman P; Kruger MC; Mallard BLThe food additive E171 (titanium dioxide, TiO2), is widely used in foods, pharmaceuticals and cosmetics. It is a fine white powder, with at least one third of its particles sized in the nanoparticulate (˂100 nm range, TiO2 NPs). The use of E171 is controversial as its relevant risk assessment has never been satisfactorily accomplished. In vitro and in vivo studies have shown dose-dependent toxicity in various organs including the liver. TiO2 NPs have been shown to induce inflammation, cell death and structural and functional changes within the liver. The toxicity of TiO2 NPs in experimental models varies between organs and according to their physiochemical characteristics and parameters such as dosage and route of administration. Among these factors, ingestion is the most significant exposure route, and the liver is a key target organ. The aim of this review is to highlight the reported adverse effects of orally administered TiO2 NPs on the liver and to discuss the controversial state of its toxicity.Item Developmentally controlled changes during Arabidopsis leaf development indicate causes for loss of stress tolerance with age(Oxford University Press on behalf of the Society for Experimental Biology, 2020-10-22) Kanojia A; Gupta S; Benina M; Fernie AR; Mueller-Roeber B; Gechev T; Dijkwel PP; Foyer CLeaf senescence is the final stage of leaf development and is induced by the gradual occurrence of age-related changes (ARCs). The process of leaf senescence has been well described, but the cellular events leading to this process are still poorly understood. By analysis of progressively ageing, but not yet senescing, Arabidopsis thaliana rosette leaves, we aimed to better understand processes occurring prior to the onset of senescence. Using gene expression analysis, we found that as leaves mature, genes responding to oxidative stress and genes involved in stress hormone biosynthesis and signalling were up-regulated. A decrease in primary metabolites that provide protection against oxidative stress was a possible explanation for the increased stress signature. The gene expression and metabolomics changes occurred concomitantly to a decrease in drought, salinity, and dark stress tolerance of individual leaves. Importantly, stress-related genes showed elevated expression in the early ageing mutant old5 and decreased expression in the delayed ageing mutant ore9. We propose that the decreased stress tolerance with age results from the occurrence of senescence-inducing ARCs that is integrated into the leaf developmental programme, and that this ensures a timely and certain death.Item Molecular and cellular mechanisms involved in tissue-specific metabolic modulation by SARS-CoV-2(Frontiers Media SA, 2022) dos Santos AAC; Rodrigues LE; Alecrim-Zeza AL; de Araújo Ferreira L; Trettel CDS; Gimenes GM; da Silva AF; Sousa-Filho CPB; Serdan TDA; Levada-Pires AC; Hatanaka E; Borges FT; de Barros MP; Cury-Boaventura MF; Bertolini GL; Cassolla P; Marzuca-Nassr GN; Vitzel KF; Pithon-Curi TC; Masi LN; Curi R; Gorjao R; Hirabara SMCoronavirus disease 2019 (COVID-19) is triggered by the SARS-CoV-2, which is able to infect and cause dysfunction not only in lungs, but also in multiple organs, including central nervous system, skeletal muscle, kidneys, heart, liver, and intestine. Several metabolic disturbances are associated with cell damage or tissue injury, but the mechanisms involved are not yet fully elucidated. Some potential mechanisms involved in the COVID-19-induced tissue dysfunction are proposed, such as: (a) High expression and levels of proinflammatory cytokines, including TNF-α IL-6, IL-1β, INF-α and INF-β, increasing the systemic and tissue inflammatory state; (b) Induction of oxidative stress due to redox imbalance, resulting in cell injury or death induced by elevated production of reactive oxygen species; and (c) Deregulation of the renin-angiotensin-aldosterone system, exacerbating the inflammatory and oxidative stress responses. In this review, we discuss the main metabolic disturbances observed in different target tissues of SARS-CoV-2 and the potential mechanisms involved in these changes associated with the tissue dysfunction.Item Glutathione depletion affects the expression of genes involved in the molecular adaptation of C2C12 myotubes to contraction : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Physiology at Massey University, Auckland, New Zealand(Massey University, 2021) Jones, Henry WarrenBackground. Impaired muscle metabolic function and atrophy are closely linked to a wide range of conditions including cancer, diabetes, and aging. Exercise is known to improve muscle metabolism and increase muscle mass, thereby having protective and therapeutic effects against such conditions. During exercise the production of reactive oxygen species (ROS) within muscle increases. These highly reactive molecules are typically balanced by antioxidants and act as signalling molecules bringing about changes in gene expression. However, if the balance between production and detoxification is lost, they can cause oxidative damage. Chronic oxidative stress can cause muscle to atrophy and impair energy metabolism, contributing to the complications of the aforementioned conditions. Glutathione (GSH) is a three amino acid peptide and one of the most abundant antioxidant molecules in muscle, protecting against oxidative damage. In addition, when oxidised by ROS, GSH may interact with and change the activity of a range of other enzymes, affecting the activation of several signalling pathways that influence the expression of genes associated with energy metabolism and antioxidant capacity. This suggests that GSH may play a role in the magnitude of muscle adaptations to exercise through redox sensitive pathways. Aim. The primary aim was to evaluate the involvement of endogenous GSH in the molecular adaptation of skeletal muscle to contractions induced by electrical stimulation (ES) in vitro. Methods. C2C12 myoblasts were cultured and differentiated into myotubes. The experimental groups consisted of controls and those depleted of GSH by a 24-hour treatment with 1 mM buthionine sulphoximine (BSO). These were then submitted to an electrical stimulation protocol of a 1 second pulse every other second of 10 V and 50 Hz for 24 hours. Cell survival was tested using exclusion technique and trypan blue dye to determine if ES or treatment with BSO effected cell viability. Hydrogen peroxide release during ES was measured using a fluorescent probe (Amplex UltraRed©) and GSH content in the myotubes was quantified using a commercial kit. RT-PCR was conducted to measure the expression of key genes associated with muscle adaptation and metabolism following contraction. The genes tested were Catalase, CPT-1B, Citrate Synthase, GLUT4, GPx1, HK2, NRF1. NRF2, PFK, PGC-1α, PPARα, PPARγ, SOD1, SOD2, Tfam, and VEGF-A. Baseline expression was compared to expression immediately following ES as well as 1 and 3 hours after stimulation had ended. Results. The ES protocol nor treatment with BSO, alone or combined, caused any significant change in cell viability when compared to controls. Cellular concentrations of total GSH were successfully depleted in C2C12 myotubes treated with BSO. GSH depletion caused an increase in H₂O₂ concentrations of treated cells, both at baseline and during ES, in comparison to control groups. GSH depletion increased the expression of PPARγ across all time points when compared to control cells and tended to increase expression of multiple genes at baseline when compared to control groups (PFK p = 0.1149, PPARα p = 0.0654, and SOD1 p = 0.086; unpaired t-test). Electrical stimulation upregulated the expression of VEGF, GLUT4, and PGC-1α irrespective of GSH treatment, along with a tendency to increase the expression of CPT-1B (p = 0.0580; two-way ANOVA). Catalase mRNA levels increased over time following ES and were further increased in GSH depleted groups. Discussion. GSH (or the absence of) may affect baseline expression of several genes known to be involved in the molecular adaptation of skeletal muscle to exercise but, following ES, GSH depletion only affected catalase expression. The effects of increased cellular H₂O₂ concentrations, both at rest and during stimulation, along with the activation of signalling pathways by contraction (e.g., MAPK, AMPK, CaMK) are likely to play a role in the changes in mRNA expression seen in this study. This may contribute to the upregulation of genes associated with angiogenesis, fatty acid metabolism, antioxidant potential, and glucose uptake. The increased activity of these signalling pathways is not dependent on GSH or are sufficient to override the lack of GSH. Conclusion. GSH depletion did not impair gene expression following ES. Although changes were seen in the absence of electrical stimulation, these may be due to acute redox signalling. Further investigation into the specific mechanisms is required to identify potential contributing factors, such as altered levels of H₂O₂ and MAPK, AMPK and CaMK signals which arise from exercise, known to modulate gene expression.