After completing a Biomedical Science degree here at UTS, I undertook a PhD in free radical biology with Professor Nicholas Hunt in the Department of Pathology, University of Sydney. Towards the end of that time and then after graduation, I worked in Roger Dean and Wendy Jessup’s group at the Heart Research Institute with a focus on low-density lipoprotein (LDL) oxidation and foam cell macrophages.
Since coming to UTS in 2000 I have maintained my work in free radical biology. My specific interest is the role of oxidative stress in chronic inflammatory diseases. Principally I now work with Brian Oliver and Hui Chen with regard to inflammatory respiratory diseases.
My teaching foci are medical physiology, human pathophysiology and internships
I am an affiliate of the Woolcock Institute of Medical Research
American Physiological Society (member)
American Thoracic Society (member)
Higher Education Reseach and Development Society of Australasia (member)
Human Anatomy and Physiology Society (member)
Society For Free Radical Research Australasia (member)
Can supervise: YES
OXIDATIVE DAMAGE/MODIFICATIONS TO PLASMA PROTEINS, CELLS AND TISSUES
How such changes to plasma proteins, cell and tissue components can contribute to disease development remains central to my research. This has included in vivo studies examing the potential of "anti-oxidants" to prevent this changes and thus block disease progression as well as in vitro studies looking at modulation of cell function upon exposure to oxidising inflammatory agents and oxidised extracellular proteins.
I am principally involved in teaching to undergraduate students enrolled in the Faculty of Science. I am one of the academic supervisors for the undergraduate internship program. I also lecture in physiology for the University of Notre Dame, Australia, graduate medical program.
Chen, H, Power, T, Hayes, C, Reyna, J & van Reyk, D 2020, 'Perceptions of Video Scenarios to Learn Human Pathophysiology Among Undergraduate Science Students', JOURNAL OF SCIENCE EDUCATION AND TECHNOLOGY.View/Download from: Publisher's site
Pan, GJ, Rayner, BS, Zhang, Y, van Reyk, DM & Hawkins, CL 2018, 'A pivotal role for NF-κB in the macrophage inflammatory response to the myeloperoxidase oxidant hypothiocyanous acid.', Archives of biochemistry and biophysics, vol. 642, pp. 23-30.View/Download from: Publisher's site
Atherosclerosis is characterised by the infiltration of macrophages at sites of inflammation within the vessel wall and the release of myeloperoxidase (MPO), which forms hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN). HOCl is a damaging oxidant implicated in the development of atherosclerosis. Preferential formation of HOSCN occurs under conditions where thiocyanate ions are elevated, as is the case in smokers. HOSCN reacts selectively with thiols, which can result in more enzyme inactivation and damage than HOCl at susceptible sites, which may contribute to atherosclerosis in smokers. In this study, we show that exposure of macrophages to HOSCN results in a time- and dose-dependent increase in the mRNA expression and release of pro-inflammatory cytokines and chemokines, including monocyte chemotactic protein 1, tumour necrosis factor alpha, and interleukins 6, 8 and 1β. At high oxidant concentrations (>200 μM), a significant loss of cellular thiols and increased cell death is observed. HOSCN-induced cytokine/chemokine expression and cell death were decreased on pharmacological inhibition of nuclear factor kappa B. These data highlight a pathway by which HOSCN could promote inflammation and the development of atherosclerosis, in the presence of supra-physiological levels of the precursor thiocyanate, which are achievable by cigarette smoking.
Chen, H, Li, G, Chan, YL, Nguyen, T, van Reyk, D, Saad, S & Oliver, BG 2018, 'Modulation of neural regulators of energy homeostasis, and of inflammation, in the pups of mice exposed to e-cigarettes.', Neuroscience letters, vol. 684, pp. 61-66.View/Download from: Publisher's site
BACKGROUND:Maternal smoking can lead to perturbations in central metabolic regulators such as neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) signalling components in offspring. With the growing interest in e-cigarettes as a tobacco replacement, this short report assessed central metabolic regulation in offspring of mouse dams exposed to e-cigarettes. We examined the impact of continuous use of e-cigarettes, and e-cigarette replacement of tobacco cigarettes during pregnancy. Supplementation of an antioxidant l-carnitine was also co-used with tobacco cigarette in the mother to determine whether the impact of maternal tobacco smoking was oxidative stress driven. METHODS:Balb/c mice were exposed to either nicotine-containing (E-cig18) or nicotine-free (E-cig0) e-cigarette aerosols or tobacco smoke (SE) prior to mating and until their pups were weaned. After mating, two SE sub-groups were changed to E-cig18 exposure (Replacement), or supplementation l-carnitine while SE was continued. Male offspring were studied at weaning age. RESULTS:The offspring of E-cig0 dams were the heaviest with the most body fat. Replacing SE with E-cig18 during pregnancy resulted in offspring with significantly less body fat. E-cig0 offspring had significantly increased mRNA expression of brain NPY and iNOS. Maternal SE upregulated mRNA expression of NPY, NPY Y1 receptor, POMC downstream components, and iNOS expression, which were normalised in Replacement offspring, but only partially normalised with maternal L-carnitine supplementation during gestation and lactation. CONCLUSIONS:Maternal exposure to either tobacco and nicotine-free e-cigarettes lead to disturbances in the level of central homeostatic control markers in offspring, suggesting that maternal exposure to e-cigarettes is not without risks.
Abdo, AI, Rayner, BS, van Reyk, DM & Hawkins, CL 2017, 'Low-density lipoprotein modified by myeloperoxidase oxidants induces endothelial dysfunction.', Redox biology, vol. 13, pp. 623-632.View/Download from: Publisher's site
Low-density lipoprotein (LDL) modified by hypochlorous acid (HOCl) produced by myeloperoxidase (MPO) is present in atherosclerotic lesions, where it is implicated in the propagation of inflammation and acceleration of lesion development by multiple pathways, including the induction of endothelial dysfunction. Thiocyanate (SCN-) ions are utilised by MPO to produce the oxidant hypothiocyanous acid (HOSCN), which reacts with LDL in a different manner to HOCl. Whilst the reactivity of HOCl-modified LDL has been previously studied, the role of HOSCN in the modification of LDL in vivo is poorly defined, although emerging evidence suggests that these particles have distinct biological properties. This is important because elevated plasma SCN- is linked with both the propagation and prevention of atherosclerosis. In this study, we demonstrate that both HOSCN- and HOCl-modified LDL inhibit endothelium-mediated vasorelaxation ex vivo in rat aortic ring segments. In vitro experiments with human coronary artery endothelial cells show that HOSCN-modified LDL decreases in the production of nitric oxide (NO•) and induces the loss of endothelial nitric oxide synthase (eNOS) activity. This occurs to a similar extent to that seen with HOCl-modified LDL. In each case, these effects are related to eNOS uncoupling, rather than altered expression, phosphorylation or cellular localisation. Together, these data provide new insights into role of MPO and LDL modification in the induction of endothelial dysfunction, which has implications for both the therapeutic use of SCN- within the setting of atherosclerosis and for smokers, who have elevated plasma levels of SCN-, and are more at risk of developing cardiovascular disease.
Bennett, D, Knight, E, Divan, A, Kuchel, L, Horn, J, van Reyk, D & Burke da Silva, K 2017, 'How do research-intensive universities portray employability strategies? A review of their websites', Australian Journal of Career Development, vol. 26, no. 2, pp. 52-61.View/Download from: Publisher's site
© Australian Council for Educational Research 2017. Employability development is a strategic priority for universities across advanced western economies. Despite this, there is no systematic study of employability development approaches internationally. In this study, we considered how universities portray employability on the public pages of their websites. We undertook website content analysis of 107 research-intensive universities in Australia, Canada, the United Kingdom and the United States. Following Farenga and Quinlan, we classified these strategies as Portfolio, Hands-off, Award and Non-embedded. Portfolio or Award strategies were the most common across all four locations; Hands-off and Non-embedded strategies were more common to US universities; and Award was more common in the United Kingdom. Universities focused on either possessional or positional approaches to employability. We advocate for a pedagogical shift towards processual approaches in which responsibility for employability development is shared.
Capistrano, SJ, van Reyk, D, Chen, H & Oliver, BG 2017, 'Evidence of Biomass Smoke Exposure as a Causative Factor for the Development of COPD.', Toxics, vol. 5, no. 4, pp. 1-16.View/Download from: Publisher's site
Chronic obstructive pulmonary disease (COPD) is a progressive disease of the lungs characterised by chronic inflammation, obstruction of airways, and destruction of the parenchyma (emphysema). These changes gradually impair lung function and prevent normal breathing. In 2002, COPD was the fifth leading cause of death, and is estimated by the World Health Organisation (WHO) to become the third by 2020. Cigarette smokers are thought to be the most at risk of developing COPD. However, recent studies have shown that people with life-long exposure to biomass smoke are also at high risk of developing COPD. Most common in developing countries, biomass fuels such as wood and coal are used for cooking and heating indoors on a daily basis. Women and children have the highest amounts of exposures and are therefore more likely to develop the disease. Despite epidemiological studies providing evidence of the causative relationship between biomass smoke and COPD, there are still limited mechanistic studies on how biomass smoke causes, and contributes to the progression of COPD. This review will focus upon why biomass fuels are used, and their relationship to COPD. It will also suggest methodological approaches to model biomass exposure in vitro and in vivo.
Chen, H, Kelly, M, Hayes, C, van Reyk, D & Herok, G 2016, 'The use of simulation as a novel experiential learning module in undergraduate science pathophysiology education', ADVANCES IN PHYSIOLOGY EDUCATION, vol. 40, no. 3, pp. 335-341.View/Download from: Publisher's site
Ismael, FO, Proudfoot, JM, Brown, BE, van Reyk, DM, Croft, KD, Davies, MJ & Hawkins, CL 2015, 'Comparative reactivity of the myeloperoxidase-derived oxidants HOCl and HOSCN with low-density lipoprotein (LDL): Implications for foam cell formation in atherosclerosis', ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, vol. 573, pp. 40-51.View/Download from: Publisher's site
Kim, CHJ, Mitchell, JB, Bursill, CA, Sowers, AL, Thetford, A, Cook, JA, van Reyk, DM & Davies, MJ 2015, 'The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice', ATHEROSCLEROSIS, vol. 240, no. 1, pp. 234-241.View/Download from: Publisher's site
Chan, YL, Saad, S, Simar, D, Oliver, B, McGrath, K, Reyk, DV, Bertrand, PP, Gorrie, C, Pollock, C & Chen, H 2015, 'Short term exendin-4 treatment reduces markers of metabolic disorders in female offspring of obese rat dams', International Journal of Developmental Neuroscience, vol. 46, pp. 67-75.View/Download from: Publisher's site
Maternal obesity imposes significant health risks in the offspring including diabetes and dyslipidemia. We previously showed that the hypoglycaemic agent exendin-4 (Ex-4) administered from weaning can reverse the maternal impact of 'transmitted disorders' in such offspring. However daily injection for six-weeks was required and the beneficial effect may lapse upon drug withdrawal. This study aimed to investigate whether short term Ex-4 treatment during suckling period in a rodent model can reverse transmitted metabolic disorders due to maternal obesity.
Maternal obesity was induced in female Sprague Dawley rats by high-fat diet feeding for 6 weeks, throughout gestation and lactation. Female offspring were treated with Ex-4 (5 μg/kg/day) between postnatal day (P) 4 and 14. Female offspring were harvested at weaning (P20). Lipid and glucose metabolic markers were measured in the liver and fat. Appetite regulators were measured in the plasma and hypothalamus.
Maternal obesity significantly increased body weight, fat mass, and liver weight in the offspring. There was an associated inhibition of peroxisomal proliferator activated receptor gamma coactivator 1α (PGC1α), increased fatty acid synthase (FASN) expression in the liver, and reduced adipocyte triglyceride lipase (ATGL) expression. It also increased the plasma gut hormone ghrelin and reduced glucagon-like peptide-1. Ex-4 treatment partially reversed the maternal impact on adiposity and impaired lipid metabolism in the offspring, with increased liver PGC1α and inhibition of FASN mRNA expression. Ex-4 treatment also increased the expression of a novel fat depletion gene a2-zinc-glycoprotein 1 in the fat tissue.
Short term Ex-4 treatment during the suckling period significantly improved the metabolic profile in the offspring from the obese mothers at weaning. Long-term studies are needed to follow such offspring to adulthood to examine the sustained effects of Ex-4 in p...
Brown, BE, Kim, CH, Torpy, FR, Bursill, CA, Mcrobb, L, Heather, AK, Davies, MJ & Van Reyk, DM 2014, 'Supplementation with carnosine decreases plasma triglycerides and modulates atherosclerotic plaque composition in diabetic apo E -/- mice.', Atherosclerosis, vol. 232, pp. 403-409.View/Download from: Publisher's site
Objective Carnosine has been shown to modulate triglyceride and glycation levels in cell and animal systems. In this study we investigated whether prolonged supplementation with carnosine inhibits atherosclerosis and markers of lesion stability in hyperglycaemic and hyperlipidaemic mice. Methods Streptozotocin-induced diabetic apo E-/- mice were maintained for 20 weeks, post-induction of diabetes. Half of the animals received carnosine (2 g/L) in their drinking water. Diabetes was confirmed by significant increases in blood glucose and glycated haemoglobin, plasma triglyceride and total cholesterol levels, brachiocephalic artery and aortic sinus plaque area; and lower body mass. Results Prolonged carnosine supplementation resulted in a significant (~20-fold) increase in plasma carnosine levels, and a significant (~23%) lowering of triglyceride levels in the carnosine-supplemented groups regardless of glycaemic status. Supplementation did not affect glycaemic status, blood cholesterol levels or loss of body mass. In the diabetic mice, carnosine supplementation did not diminish measured plaque area, but reduced the area of plaque occupied by extracellular lipid (~60%) and increased both macrophage numbers (~70%) and plaque collagen content (~50%). The area occupied by a-actin-positive smooth muscle cells was not significantly increased. Conclusions These data indicate that in a well-established model of diabetes-associated atherosclerosis, prolonged carnosine supplementation enhances plasma levels, and has novel and significant effects on atherosclerotic lesion lipid, collagen and macrophage levels. These data are consistent with greater lesion stability, a key goal in treatment of existing cardiovascular disease. Carnosine supplementation may therefore be of benefit in lowering triglyceride levels and suppressing plaque instability in diabetes-associated atherosclerosis.
Ang, K & Van Reyk, DM 2013, ''Teach Me Chemistry Like a Ladder and Make it Real' - Barriers and Motivations Students Face in Learning Chemistry for Bioscience', International Journal of Innovation in Science and Mathematics Education, vol. 21, no. 2, pp. 1-12.
Students enrolled in the Bachelor of Nursing program come with diverse academic abilities, age, language skills and experience. Many enrol without any prior knowledge of the supporting sciences including chemistry. Moreover, whilst some do possess such prior knowledge, they may have had a substantial break since they last studied chemistry. This paper draws from surveys and interviews conducted to investigate students prior knowledge of chemistry and experiences around learning. These were first year students enrolled in a core unit of anatomy and physiology for which, albeit implicitly some prior knowledge of chemistry is assumed. It explores barriers and motivations to learning chemistry and offers insights into what students need in order to gain a mastery of the foundational chemical principles that underlie anatomy and physiology. This research is of considerable importance given that the teaching of anatomy and physiology relies heavily on foundation-level chemistry knowledge. It is of great significance if students can be better supported in the successful learning, retention and completion of their nursing studies. Insights reveal that problems stem from various factors including length of time since their last chemistry studies, language difficulties, students interests and motivations in the subject, pace and structure of sessions, relevance of information and the students ability to manage the amount of content. This informs future practice suggesting that it is important to scaffold the learning for all students in a structured and relevant manner. Additionally, it supports the development and provision of resources to support students transitioning into higher education from diverse backgrounds
Rathner, JA, van Reyk, D & Crane, JW 2013, 'Editorial', International Journal of Innovation in Science and Mathematics Education, vol. 21, no. 3.
Rathner, JA, van Reyk, D & Crane, JW 2013, 'Editorial-volume 21, numbers 2 & 3', International Journal of Innovation in Science and Mathematics Education, vol. 21, no. 2.
Moheimani, F, Kim, CH, Suryo Rahmanto, A, Van Reyk, DM & Davies, MJ 2012, 'Inhibition of lysosomal function in macrophages incubated with elevated glucose concentrations: A potential contributory factor in diabetes-associated atherosclerosis', Atherosclerosis, vol. 223, no. 1, pp. 144-151.View/Download from: Publisher's site
Objective People with diabetes have an elevated risk of atherosclerosis. The accumulation of lipid within macrophage cells in the artery wall is believed to arise via the uptake and subsequent processing of modified low-density lipoproteins (LDL) via the endo-lysosomal system. In this study the effects of prolonged exposure to elevated glucose upon macrophage lysosomal function was examined to determine whether this contributes to modulated protein catabolism. Methods Human monocytes were isolated from white-cell concentrates and differentiated, in vitro, into monocyte-derived macrophages over 11 days in medium containing 530 mmol/L glucose. Murine macrophage-like J774A.1 cells were incubated similarly. Lysosomal cathepsin (B, D, L and S) and acid lipase activities were assessed using fluorogenic substrates; cathepsin protein levels were examined by Western blotting. Lysosomal numbers were examined using the lysomotropic fluorescent dye LysoTracker DND-99, measurement of aryl sulfatase activity, and quantification of lysosome-associated membrane glycoprotein-1 (LAMP-1) by Western blotting. Results Exposure to elevated glucose, but not mannitol, resulted in a concentration-dependent decrease in the activity, and to a lesser extent protein levels, of four lysosomal cathepsins. Acid lipase activity was also significantly reduced. Arysulfatase activity, LAMP-1 levels and lysosomal numbers were also decreased at the highest glucose concentrations, though to a lesser extent.
Moheimani, F, Tan, JT, Brown, BE, Heather, AK, Van Reyk, DM & Davies, MJ 2011, 'Effect of exposure of human monocyte-derived macrophages to high, versus normal, glucose on subsequent lipid accumulation from glycated and acetylated low-density lipoproteins', Experimental Diabetes Research, vol. 2011, no. 851280, pp. 1-10.View/Download from: Publisher's site
This is the second paper from Dr Moheimani's PhD thesis of which David van Reyk was a co-supervisor in his role as Visiting HRI Fellow. It examines the mechanisms that promote and accelerate the development and progression of atherosclerosis in people with diabetes
Moheimani, F, Morgan, PE, Van Reyk, DM & Davies, MJ 2010, 'Deleterious effects of reactive aldehydes and glycated proteins on macrophage proteosomal function: Possible links between diabetes and atherosclerosis', Biochimica et Biophysica acta, vol. 1802, no. 6, pp. 561-571.
People with diabetes experience chronic hyperglycemia and are at a high risk of developing atherosclerosis and microvascular disease. Reactions of glucose, or aldehydes derived from glucose (e.g. methylglyoxal, glyoxal, or glycolaldehyde), with proteins result in glycation that ultimately yield advanced glycation end products (AGE). AGE are present at elevated levels in plasma and atherosclerotic lesions from people with diabetes, and previous in vitro studies have postulated that the presence of these materials is deleterious to cell function. This accumulation of AGE and glycated proteins within cells may arise from either increased formation and/or ineffective removal by cellular proteolytic systems, such as the proteasomes, the major multi-enzyme complex that removes proteins within cells. In this study it is shown that whilst high glucose concentrations fail to modify proteasome enzyme activities in J774A.1 macrophage-like cell extracts, reactive aldehydes enhanced proteasomal enzyme activities. In contrast BSA, pre-treated with high glucose for 8 weeks, inhibited both the chymotrypsin-like and caspase-like activities. BSA glycated using methylglyoxal or glycolaldehyde, also inhibited proteasomal activity though to differing extents. This suppression of proteasome activity by glycated proteins may result in further intracellular accumulation of glycated proteins with subsequent deleterious effects on cellular function.
Lloyd, MM, Van Reyk, DM, Davies, MJ & Hawkins, CL 2008, 'Hypothiocyanous acid is a more potent inducer of apoptosis and protein thiol depletion in murine macrophage cells than hypochlorous acid or hypobromous acid', Biochemical Journal, vol. 414, pp. 271-280.View/Download from: Publisher's site
Hypohalous acids are generated by activated leucocytes, via the formation of H2O2 and the release of peroxidase enzymes (myeloperoxidase and eosinophil peroxidase). These species are important bactericidal agents, but HOCI (hypoclorous acid) and HOBr (hypobromous acid) have also bee implicated in tissue damage in a number of inflammatory diseases. HOSCN (hypothiocyanous acid; cyanosulfenic acid) us a milder more thiol-specific, oxidant than HOCI or HOBr and as such may be a more potent inducer of cellular dysfunction due to selective targerting of critical thiol residues on proteins. In the present study, HOCI and HOBr are shown to react rapidly with macrophage (J774A.1) cells, resulting in a greater extent if cell lysis compared with HOSCN. However, HOSCN induces apoptosis and necrosis with greater efficacy and at lower concentrations, than HOCI or HOBr.
Brown, B, Rashid, I, Van Reyk, DM & Davies, MJ 2007, 'Glycation of low-density lipoprotein results in the time- dependent accumulation of cholesteryl esters and apolipoprotein B-100 protein in primary human monocyte-derived macrophages', FEBS Journal, vol. 274, no. 6, pp. 1530-1540.View/Download from: Publisher's site
Nonenzymatic covalent binding (glycation) of reactive aldehydes (from glucose or metabolic processes) to low-density lipoproteins has been previously shown to result in lipid accumulation in a murine macrophage cell line. The formation of such lipid-laden cells is a hallmark of atherosclerosis. In this study, we characterize lipid accumulation in primary human monocyte-derived macrophages, which are cells of immediate relevance to human atherosclerosis, on exposure to low-density lipoprotein glycated using methylglyoxal or glycolaldehyde. The time course of cellular uptake of low-density lipoprotein-derived lipids and protein has been characterized, together with the subsequent turnover of the modified apolipoprotein B-100 (apoB) protein. Cholesterol and cholesteryl ester accumulation occurs within 24 h of exposure to glycated low-density lipoprotein, and increases in a time-dependent manner. Higher cellular cholesteryl ester levels were detected with glycolaldehyde-modified low-density lipoprotein than with methylglyoxal-modified low-density lipoprotein. Uptake was significantly decreased by fucoidin (an inhibitor of scavenger receptor SR-A) and a mAb to CD36.
Rashid, I, Van Reyk, DM & Davies, MJ 2007, 'Carnosine and its constituents inhibit glycation of low-density lipoproteins that promotes foam cell formation in vitro', FEBS Letters, vol. 581, no. 5, pp. 1067-1070.View/Download from: Publisher's site
Gycation of low-density lipoprotein (LDL) by reactive aldehydes, such as glycolaldehyde, can resultin the cellular accumulation of cholesterol in macrophages. In this study, it is shown that carnosis, or its constituent amino acids beta-alanine and L-histidine, can inhibit the modification of LDL by glycolaldehyde when prsent at equimolar concentrations to the modifying agent,. This protective effect was accompanied by inhibition of cholesterol and cholesteryl ester accumulation in human monocyte-derived macrophages incubated with the glycated LDL. This carnosine and its constituent amino acids may have therapeutic potential in preventing diabetes-induced atherosclerosis.
Brown, B, Mahroof, F, Cook, N, Van Reyk, DM & Davies, MJ 2006, 'Hydrazine compounds inhibit glycation of low-density lipoproteins and prevent the in vitro formation of model foam cells from glycolaldehyde-modified low-density lipoproteins', Diabetologia, vol. 49, no. 4, pp. 775-783.View/Download from: Publisher's site
Aims/hypothesis: Previous studies have shown that glycation of LDL by methylglyoxal and glycolaldehyde, in the absence of significant oxidation, results in lipid accumulation in macrophage cells. Such foam cells are a hallmark of atherosclerosis. In this
Van Reyk, DM, Brown, A, Hults'en, LM, Dean, R & Jessup, W 2006, 'Oxysterols in biological systems: sources, metabolism and pathophysiological relevances', Redox Report, vol. 11, no. 6, pp. 255-262.View/Download from: Publisher's site
Oxysterols are the 27-carbon products of cholesterol by both enzymic and non-enzymic mechanisms. Their roles in cholesterol homeostasis, as well as in diseases in which oxidative damage and lipid peroxidation are implicated (e.g. atherosclerosis), have been investigated extensively. However, there are a number of important considerations regarding the chysiological/pathophysiological functions and activities of the different oxysterols. First,in both normal and diseased tissues, the levels of oxysterols are very low when compared to the native sterol. Also, when assessing studies thathave measured the levels of oxysterols in biological samples, there must be careful consideration as to the method of sample isolation,s torage and sampling. This is because of the potential generation or loss of oxysterols during these procedures. Additionally, the relevance of in vitro studies which examine the effects of oxysterols upon cell function should be judged as to cellular oxysterol content (both in terms of the levels of oxysterol and the degree of esterification) resulting fromthe oxysterol treatment. We present evidence that the means by which oxysterol is delivered in vitro determines whether the oxyterol content reflects what has been found in vivo. Studies identifying the specific cellular targets of oxysterol indicate that several oxysterols may be regulators of cellular lipid metabolism via control of gene transcription.
Hultén, LM, Ullström, C, Krettek, A, Van Reyk, D, Marklund, SL, Dahlgren, C & Wiklund, O 2005, 'Human macrophages limit oxidation products in low density lipoprotein', Lipids in Health and Disease, vol. 4.View/Download from: Publisher's site
This study tested the hypothesis that human macrophages have the ability to modify oxidation products in LDL and oxidized LDL (oxLDL) via a cellular antioxidant defence system. While many studies have focused on macrophage LDL oxidation in atherosclerosis development, less attention has been given to the cellular antioxidant capacity of these cells. Compared to cell-free controls (6.2 ± 0.7 nmol/mg LDL), macrophages reduced TBARS to 4.42 ± 0.4 nmol/mg LDL after 24 h incubation with LDL (P = 0.022). After 2 h incubation with oxLDL, TBARS were 3.69 ± 0.5 nmol/mg LDL in cell-free media, and 2.48 ± 0.9 nmol/mg LDL in the presence of macrophages (P = 0.034). A reduction of lipid peroxides in LDL (33.7 ± 6.6 nmol/mg LDL) was found in the presence of cells after 24 h compared to cell-free incubation (105.0 ± 14.1 nmol/mg LDL) (P = 0.005). The levels of lipid peroxides in oxLDL were 137.9 ± 59.9 nmol/mg LDL and in cell-free media 242 ± 60.0 nmol/mg LDL (P = 0.012). Similar results were obtained for hydrogen peroxide. Reactive oxygen species were detected in LDL, acetylated LDL, and oxLDL by isoluminol-enhanced chemiluminescence (CL). Interestingly, oxLDL alone gives a high CL signal. Macrophages reduced the CL response in oxLDL by 45% (P = 0.0016). The increased levels of glutathione in oxLDL-treated macrophages were accompanied by enhanced catalase and glutathione peroxidase activities. Our results suggest that macrophages respond to oxidative stress by endogenous antioxidant activity, which is sufficient to decrease reactive oxygen species both in LDL and oxLDL. This may suggest that the antioxidant activity is insufficient during atherosclerosis development. Thus, macrophages may play a dual role in atherogenesis, i.e. both by promoting and limiting LDL-oxidation. © 2005 Hultén et al; licensee BioMed Central Ltd.
van Reyk, D, Sarel, S & Hunt, N 2000, 'Inhibition of in vitro lymphoproliferation by three novel iron chelators of the pyridoxal and salicyl aldehyde hydrazone classes', BIOCHEMICAL PHARMACOLOGY, vol. 60, no. 4, pp. 581-587.View/Download from: Publisher's site
van Reyk, DM & Jessup, W 1999, 'The macrophage in atherosclerosis: modulation of cell function by sterols', JOURNAL OF LEUKOCYTE BIOLOGY, vol. 66, no. 4, pp. 557-561.
van Reyk, DM, Jessup, W & Dean, RT 1999, 'Prooxidant and antioxidant activities of macrophages in metal-mediated LDL oxidation - The importance of metal sequestration', ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, vol. 19, no. 4, pp. 1119-1124.View/Download from: Publisher's site
James, MJ, van Reyk, D, Rye, KA, Dean, RT, Cleland, LG, Barter, PJ & Jessup, W 1998, 'Low density lipoprotein of synovial fluid in inflammatory joint disease is mildly oxidized', LIPIDS, vol. 33, no. 11, pp. 1115-1121.View/Download from: Publisher's site
Garner, B, Van Reyk, D, Dean, RT & Jessup, W 1997, 'Direct copper reduction by macrophages: Its role in low density lipoprotein oxidation', Journal of Biological Chemistry, vol. 272, no. 11, pp. 6927-6935.View/Download from: Publisher's site
Oxidation of low density lipoprotein (LDL) results in changes to the lipoprotein that are potentially atherogenic. Numerous studies have shown that macrophages cultured in vitro can promote LDL oxidation via a transition metal-dependent process, yet the exact mechanisms that are responsible for macrophage-mediated LDL oxidation are not understood. One contributing mechanism may be the ability of macrophages to reduce transition metals. Reduced metals (such as Fe(II) or Cn(I)) rapidly react with lipid hydroperoxides, leading to the formation of reactive lipid radicals and conversion of the reduced metal to its oxidized form. We demonstrate here the ability of macrophages to reduce extracellular iron and copper and identify a contributing mechanism. Evidence is provided that a proportion of cell- mediated metal reduction is due to direct transplasma membrane electron transport. Glucagon suppressed both macrophage-mediated metal reduction and LDL oxidation. Although metal reduction was augmented when cells were provided with a substrate for thiol production, thiol export was not a strict requirement for cell-mediated metal reduction. Similarly, while the metal- dependent acceleration of LDL oxidation by macrophages was augmented by thiol production, macrophages could still promote LDL oxidation when thiol export was minimized (by substrate limitation). This study identifies a novel mechanism that may contribute to macrophage-mediated LDL oxidation and may also reveal potential new strategies for the inhibition of this process.
VanReyk, DM & Dean, RT 1996, 'The iron-selective chelator desferal can reduce chelated copper', FREE RADICAL RESEARCH, vol. 24, no. 1, pp. 55-60.View/Download from: Publisher's site
VANREYK, DM, BROWN, AJ, JESSUP, W & DEAN, RT 1995, 'BATCH-TO-BATCH VARIATION OF CHELEX-100 CONFOUNDS METAL-CATALYZED OXIDATION, LEACHING OF INHIBITORY COMPOUNDS FROM A BATCH OF CHELEX-100 AND THEIR REMOVAL BY A PRE-WASHING PROCEDURE', FREE RADICAL RESEARCH, vol. 23, no. 6, pp. 533-535.View/Download from: Publisher's site
VANREYK, DM, SAREL, S & HUNT, NH 1992, 'INVITRO EFFECTS OF 3 IRON CHELATORS ON MITOGEN-ACTIVATED LYMPHOCYTES - IDENTIFICATION OF DIFFERENCES IN THEIR MECHANISMS OF ACTION', INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY, vol. 14, no. 5, pp. 925-932.View/Download from: Publisher's site
Armati, PJ, Pollard, JD, Van Reyk, D & Van der Lubbe, L 1988, 'Neuroimmunological electron microscopy with microwave-accelerated fixation', Journal of Immunological Methods, vol. 110, no. 2, pp. 267-269.View/Download from: Publisher's site
Immunoelectron microscopy is an important tool used to determine the precise location of immune complexes. Standard concentrations of glutaraldehyde destroy these complexes. This paper describes a method in which the period of glutaraldehyde fixation is shortened by concomitant microwave treatment. Using 1.25% glutaraldehyde and microwave fixation ideal preservation and demonstration of MHC class I antigen on Schwann cells was obtained by the peroxidase method. © 1988.
Rashid, I, Brown, B, Van Reyk, DM & Davies, MJ 2006, 'The roles of protein glycation, glycoxidation and advanced glycation end-product formation in diabetes-induced atherosclerosis' in Kaur Sukhinder, C (ed), Biochemistry of Atherosclerosis, Springer, New York, USA, pp. 247-283.
Diabetes is known to induce a range of micro-and macrovascular compliacations with the latter resutling in premature and accelerated atherosclerosis. Thus people with diabetes have a 2-4 fold increased risk of developing cardiovascular diseases which is responsible for ca. 50% of deaths amongst people with diabetes. The mechanisms behind this elevated risk are still not fully understood, though there is now increasing evidence for a role of glycation and clycoxidation reactions induced by hyperglycemia. This article reviews current knowledge of the role that these reactions play in diabetes-induced atherosclerosis with particular emphasis on the molecular reactions that result in the modification of lipoproteins, and the consequences of these reactions on cellular metabolism.
van Reyk, D, Oliver, B, Capistrano, S, Komalla, V, Haghi, M & Zosky, G 2019, 'Pro-inflammatory effects of exposure of the combination of silicon- and iron-containing particles upon human lung fibroblasts', EUROPEAN RESPIRATORY JOURNAL, European-Respiratory-Society (ERS) International Congress, EUROPEAN RESPIRATORY SOC JOURNALS LTD, Madrid, SPAIN.View/Download from: Publisher's site
Abdo, AI, Rayner, BS, van Reyk, DM & Hawkins, CL 2016, 'Modification of Low-Density Lipoprotein by Myeloperoxidase Oxidants - a Pathway to Endothelial Dysfunction in Atherosclerosis?', FREE RADICAL BIOLOGY AND MEDICINE, ELSEVIER SCIENCE INC, pp. S72-S72.View/Download from: Publisher's site
Van Reyk, DM & Ang, K 2013, 'Is H+ the symbol for acid? Provision of learning support in foundation-level chemistry for Bachelor of Nursing students enrolled in bioscience subjects', International First Year in Higher Education (FYHE) 16th Conference, First Year in Higher Education Centre, Wellington.
Despite the value given to the teaching of bioscience as a central component of undergraduate nursing education, it has been accepted that nursing students often find bioscience subjects some of the most difficult to both master and perform well in. This nuts and bolts paper explores a practical approach undertaken to give first year students, commencing their anatomy and physiology unit, the opportunity to self-assess their existing knowledge of chemistry. We then evaluated the outcomes of a providing a wiki of student-sourced web pages on chemistry that students could use to address any knowledge gaps or revise aspects of basic chemistry. We found that students were open to using online resources provided they saw the relevance, were aware of them and had time and access to tools. Additionally, results also indicated that encouragement from teaching staff may drive the usage of self-directed online resources.
Ismael, F, van Reyk, DM, Davies, MJ & Hawkins, CL 2010, 'The Role of Low-density Lipoprotein Modification by Thiocyanate-derived Oxidants in Atherosclerosis', FREE RADICAL BIOLOGY AND MEDICINE, 17th Annual Meeting of the Society-for-Free-Radical-Biology-Medicine /15th Biennial Meeting of the Society-for-Free-Radical-Research-International, ELSEVIER SCIENCE INC, Orlando, FL, pp. S22-S22.View/Download from: Publisher's site
Moheimani, F, van Reyk, DM & Davies, MJ 2008, 'Do glucose and reactive aldehydes modulate the removal of glycated proteins by proteasomes?', ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 9th Annual Conference on Arteriosclerosis, Thrombosis and Vascular Biology, LIPPINCOTT WILLIAMS & WILKINS, Atlanta, GA, pp. E100-E100.
Lloyd, M, van Reyk, D, Davies, M & Hawkins, C 2007, 'HOSCN is a more potent inducer of apoptosis and protein thiol depletion in murine macrophage cels than HOCl or HOBr', FREE RADICAL BIOLOGY AND MEDICINE, 14th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine, ELSEVIER SCIENCE INC, Washington, DC, pp. S77-S77.
Van Reyk, DM, Brown, AJ, Hult'en, LM, Hart, PH, Dean, RT & Jessup, W 2002, 'Lipoprotein-delivered oxysterols do not stimulate cytokine production in macrophage foam cells at pathophysiologically relevant levels', CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Joint Symposium of the Australian-Athersclerosis-Society/Australian-Vascular-Biology-Society, BLACKWELL PUBLISHING ASIA, MELBOURNE, AUSTRALIA, pp. A18-A18.
Jessup, W, vanReyk, D & Dean, RT 1997, 'Pro- and anti-oxidant activities of macrophages in LDL oxidation: The importance of metal sequestration', ATHEROSCLEROSIS, ELSEVIER SCI IRELAND LTD, pp. 211-212.View/Download from: Publisher's site
HUNT, NH, VANREYK, DM, FRAGONAS, JC, JEITNER, TM & GOLDSTONE, SD 1970, 'REDOX MECHANISMS IN T-CELL ACTIVATION', OXIDATIVE STRESS, CELL ACTIVATION AND VIRAL INFECTION, International Meeting on Oxidative Stress, Cell Activation and Viral Infection, BIRKHAUSER VERLAG, MINIST RES, PARIS, FRANCE, pp. 237-251.