SUNScholar - Browsing by Author "Van Rensburg, S. J."

Browsing by Author "Van Rensburg, S. J."

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Changes in erythrocyte membrane fatty acids during a clinical trial of eicosapentaenoic acid (EPA) supplementation in schizophrenia
(2009) Van Rensburg, S. J.; Smuts, C. M.; Hon, D.; Kidd, M.; Van Der Merwe, S.; Myburgh, C.; Oosthuizen, P.; Emsley, R.
In a previously reported double-blind, placebo-controlled trial of eicosapentaenoic acid (EPA) as supplemental treatment in 40 patients with schizophrenia, we found significant improvement in symptoms as measured by the Positive and Negative Syndrome Scale (PANSS) compared to placebo (Emsley et al. 2002). Here we report changes in fatty acid composition of erythrocyte membranes in the same sample (n∈=∈16 in each group). After 12 weeks of receiving EPA, levels of several saturated and mono-unsaturated fatty acids decreased significantly while levels of n-3 fatty acids increased significantly compared to the placebo group. Increases of n-3 and n-6 fatty acids in the erythrocyte membranes were greater in subjects who improved more than 20% on overall symptoms. Changes in fatty acids correlated significantly with improvement in PANSS sub-scale scores, more so in females than in males. Docosahexaenoic acid (DHA) (22:6n-3) levels increased less than expected, suggesting a possible defect in synthesis or incorporation of DHA into membranes in schizophrenia. Improvement in dyskinesia correlated significantly with an increase in alpha-linolenic acid (18:3n-3; p∈=∈0.03), and a decrease in 20:1n-9 (p∈=∈0.005). © 2009 Springer Science+Business Media, LLC.
Erythrocyte membrane fatty acids in patients with multiple sclerosis
(2009) Hon, G. M.; Hassan, M. S.; Van Rensburg, S. J.; Abel, S.; Marais, D. W.; Van Jaarsveld, P.; Smuts, C. M.; Henning, F.; Erasmus, R. T.; Matsha, T.
Background: Reports on fatty acids levels in multiple sclerosis remain inconclusive. Objective: To determine the erythrocyte membrane fatty acid levels in multiple sclerosis patients and correlate with Kurtzke Expanded Disability Status Scale. Methods: Fatty acid composition of 31 multiple sclerosis and 30 control individuals were measured by gas chromatography. Results: The membrane phosphatidylcholine C20:4 n-6 concentration was lower in the multiple sclerosis patients when compared to that of the control group, P = 0.04 and it correlated inversely with the EDSS and FSS. Conclusion: Decrease in C20:4 n-6 in the erythrocyte membrane could be an indication of depleted plasma stores, and a reflection of disease severity.
Immune cell membrane fatty acids and inflammatory marker, C-reactive protein, in patients with multiple sclerosis
(2009) Hon, G.; Hassan, M.; Van Rensburg, S. J.; Abel, S.; Marais, D. W.; Van Jaarsveld, P.; Smuts, C.; Henning, F.; Erasmus, R.; Matsha, T.
Measurement of fatty acids in biological fluids and cell membranes including leucocytes from multiple sclerosis patients is inconsistent. The objective of the present study was to investigate the fatty acid composition within the different membrane phospholipid fractions in peripheral blood mononuclear cells in multiple sclerosis patients, and correlate with severity of neurological outcome as measured by the Kurtzke Expanded Disability Status Scale and Functional System Scores. The fatty acid composition of phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, sphingomyelin and phosphatidylinositol phospholipids in the peripheral blood mononuclear cells of twenty-six multiple sclerosis and twenty-five control subjects were measured by GC, and C-reactive protein was measured in all subjects. The elongation product of 20:4n-6, 22:4n-6, was significantly decreased in membrane phosphatidylethanolamine and phosphatidylserine in multiple sclerosis patients (P=0.01 and P=0.03 respectively), and correlated inversely with severity of disease and C-reactive protein. Also an inverse correlation was observed between the C-reactive protein and membrane phosphatidylcholine and phosphatidylserine 20:4n-6. Cultural and ethnic differences, as well as dietary variability, especially in a diseased state have been implicated in the differences observed in the fatty acid composition in peripheral blood mononuclear cell membranes of patients with multiple sclerosis. The present results suggest that the disease state may in part explain the reported inconsistencies in fatty acid levels in multiple sclerosis patients.
Membrane saturated fatty acids and disease progression in Multiple Sclerosis patients
(2009) Hon, G. M.; Hassan, M. S.; Van Rensburg, S. J.; Abel, S.; Erasmus R. T.; Matsha, T.
The risk of developing multiple sclerosis is associated with increased dietary intake of saturated fatty acids. We determined the fatty acid composition within the different phospholipid fractions of red blood and peripheral blood mononuclear cell membranes of 31 patients diagnosed with multiple sclerosis and 30 healthy control subjects using gas chromatography. Individual saturated fatty acids were correlated with the severity of neurological outcome as measured by the Kurtzke Expanded Disability Status Scale. Significant increases were found in multiple sclerosis peripheral blood mononuclear cell membrane sphingomyelin C14:0 and phosphatidylinositol C22:0. In the peripheral blood mononuclear cell membranes, C22:0 and C24:0 showed positive correlations, while C14:0, C16:0 and C20:0 showed inverse correlations with the Functional System Scores. In conclusion, this study is in accordance with previous studies that have shown an increase in shorter long-chain SATS in MS patients. In addition, this study also showed that higher C14:0 and C16:0 reflected better disease outcome as demonstrated by the inverse correlation with the EDSS and FSS. We have also characterized the specific SATS, that is, long-chain SATS that may increase the risk of developing MS. © 2009 Springer Science+Business Media, LLC.
Monounsaturated fatty acids in blood cell membranes from patients with multiple sclerosis
(2011) Hon, G. M.; Hassan, M. S.; Van Rensburg, S. J.; Abel, S.; Erasmus, R. T.; Matsha, T.
The aim of this study was to investigate whether blood cell membrane monounsaturated fatty acids were associated with inflammation and disease outcome in patients with multiple sclerosis. The fatty acid composition in peripheral blood mononuclear cell and red blood cell membranes from 26 patients and 25 controls were determined by gas chromatography. Results showed positive associations between C-reactive protein and C16:1n-7, C18:1n-7, and C24:1n-9 in membranes from controls only. In general, C18:1n-9 and C20:1n-9 showed inverse correlations, while C16:1n-7 and C18:1n-7 showed positive correlations with disease outcome. Multiple sclerosis has a known inflammatory component. There is scarcity of literature on the role of monounsaturated fatty acids in inflammation, but results from this study suggested an association in healthy subjects between monounsaturated fatty acids and C-reactive protein, even at physiologically low levels. This association was not found in the plasma from patients. Furthermore, the n-9 and n-7 fatty acids played different roles in disease outcome, and therefore warrant inclusion, together with polyunsaturated fatty acids when investigating the inflammatory aspects of the disease.
A new model for the pathophysiology of Alzheimer's disease : aluminium toxicity is exacerbated by hydrogen peroxide and attenuated by an amyloid protein fragment and melatonin
(Health & Medical Publishing Group, 1997) Van Rensburg, S. J.; Daniels, W. M. U.; Potocnik, F. C. V.; Van Zyl, J. M.; Taljaard, J. J. F.; Emsley, R. A.
Objectives. Although Alzheimer's disease (AD) is the leading cause of dementia in developed countries, there is an as yet unexplained lower prevalence of the disease in parts of Africa. AD is characterised by a catastrophic loss of neurons; free radicals (oxidative toxins) have been implicated in the destruction of the cells through the process of lipid peroxidative damage of cell membranes, previously aluminium (Al) and a fragment of beta amyloid (Aβ 25-35) were shown to exacerbate free-radical damage, while melatonin reduced this effect. The aim of the present study was: (i) to investigate the conditions determining the toxicity of Al and Aβ 25-35; and (ii) to assess whether melatonin could attenuate the damage done by both aluminium and the amyloid fragment, thus suggesting a pathway for the aetiology of AD. Design. An in vitro model system was used in which free radicals were generated, causing lipid peroxidation of platelet membranes, thus simulating the disease process found in the brain. Results. 1. Al and Aβ 25-35 caused lipid peroxidation in the presence of the iron (II) ion (Fe2+), Al being more toxic than Aβ 25-35. 2. Aβ 25-35 attenuated the lipid peroxidation promoted by Al. 3. Hydrogen peroxide (H2O2) greatly exacerbated the toxicity of Al and Aβ 25-35. 4. Melatonin prevented lipid peroxidation by Al and Aβ 25-35 in the absence of H2O2, but only reduced the process when H2O2 was present. Conclusions. In the light of the results obtained from the present study, the following hypotheses are formulated. 1. In AD, excessive quantities of Al are taken up into the brain, where the Al exacerbates iron-induced lipid peroxidation in the lysosomes. 2. In response, the normal synthetic pathway of amyloid protein is altered to produce Aβ fragments which attenuate the toxicity of Al. In the process of sequestering the Al and iron, immature plaques are formed in the brain. 3. Microglia are activated, in an attempt to destroy the plaques by secreting reactive oxygen species such as H2O2. At this point in the disease process, lipid peroxidation causes a catastrophic loss of brain cells. 4. Melatonin, together with other free radical scavengers in the brain, reduces the free-radical damage caused by Al and Aβ, except in the latter stages of the disease process. Since melatonin is produced by the pineal gland only in the dark, the excess of electric light in developed countries may help explain why AD is more prevalent in these countries than in rural Africa.
Non-esterified fatty acids in blood cell membranes from patients with multiple sclerosis
(2012) Hon, G. M.; Hassan, M. S.; Van Rensburg, S. J.; Abel, S.; Erasmus, R. T.; Matsha, T.
The literature on non-esterified fatty acid (NEFA) concentrations in blood cell membranes from patients with multiple sclerosis (MS) is scarce and reports on concentrations in brain tissue from these patients are inconsistent. NEFAs are needed for several biological functions, for example, as precursors for inflammatory eicosanoid synthesis. The objective of this study was therefore to compare NEFA concentrations in blood cell membranes from patients with that of healthy control subjects, and to correlate possible changes with disease outcome. NEFA C18:2n-6 (9,12-octadecadienoic acid) was decreased in peripheral blood mononuclear cell membranes from patients, median (quartile range): patients: 0.05 (0.02) and controls: 0.07 (0.14)μg/mg protein, p=0.007. C18:2n-6 also showed a weaker relationship with other fatty acids: with C16:0: patients: R=0.40, p=0.04; controls: R=0.82, p=0.000001. Saturated and MUFA showed positive correlations with the Bowel and bladder Functional System Scores (FSS). In contrast, in red blood cell membranes C18:2n-6 and C22:0 (docosanoic acid) showed inverse correlations with the Sensory and Brainstem FSS. The decrease in NEFA C18:2n-6 resulted in metabolic abnormalities between itself and saturated and monounsaturated NEFAs. Altered fatty acid composition in immune cell membranes would influence immune cell functions, and could possibly have contributed to the positive correlations between these fatty acids and disease outcome. © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Peripheral blood mononuclear cell membrane fluidity and disease outcome in patients with multiple sclerosis
(2012) Hon, G. M.; Hassan, M. S.; Van Rensburg, S. J.; Abel, S.; Erasmus, R. T.; Matsha, T.
Immune cell membrane lipids are important determinants of membrane fluidity, eicosanoid production and phagocytosis and fatty acid metabolic abnormalities have been reported in immune cells from patients with multiple sclerosis. The aim of this study was to investigate the relationship between peripheral blood mononuclear cell membrane fluidity, permeability status, and disease outcome as measured by the Kurtzke expanded disability status scale. Phospholipids, fatty acids and cholesterol composition in peripheral blood mononuclear cells from 26 patients diagnosed with multiple sclerosis and 25 healthy control subjects were determined by colorimetric assay, gas chromatography and enzymatic assays, respectively. Membrane fluidity was calculated according to previously established formulae and correlated with C-reactive protein and the Kurtzke expanded disability status scale. There were no significant differences in membrane lipids in peripheral blood mononuclear cells from patients and controls. However, correlation studies showed lipid metabolic abnormalities, which were reflected in significant correlations between membrane fluidity as measured by both its fatty acid and phospholipid compositions, and the functional system scores. C-reactive protein showed positive correlations with phosphatidylcholine, phosphatidylserine, phosphatidylinositol and total phospholipids in membranes from control subjects. Metabolic abnormalities, as well as correlations between membrane fluidity and the functional system scores, suggested the involvement of these immune cell membranes in the disease progression. Furthermore, the changed relationship between membrane phospholipids and C-reactive protein, which has been shown to correlate with infectious episodes and clinical relapse, could be an indication of immune cell dysfunction in patients with multiple sclerosis. © 2011 Indian Society of Haematology & Transfusion Medicine.
Plasma non-esterified fatty acids in patients with multiple sclerosis
(2011) Hon, G. M.; Hassan, M. S.; Van Rensburg, S. J.; Abel, S.; Erasmus, R. T.; Matsha, T.
Zinc and platelet membrane microviscosity in Alzheimer's disease. The in vivo effect of zinc on platelet membranes and cognition
(Health & Medical Publishing Group, 1997) Potocnik, F. C. V.; Van Rensburg, S. J.; Park, C.; Taljaard, J. J. F.; Emsley, R. A.
Objectives. To investigate the effects of oral zinc supplementation on: (i) plasma zinc concentrations; (ii) platelet membrane microviscosity in vivo; and (iii) cognitive function of Alzheimer's disease (AD) patients. Design. An open-labelled pilot study. Setting. University of Stellenbosch Medical School and Stikland Hospital. Subjects. Six volunteer AD patients. Outcome measures. Plasma zinc levels, platelet membrane microviscosity and cognition (MMSE and ADAS-cog tests). Results. Oral zinc supplementation (30 mg/day) did not increase plasma zinc levels significantly, but significantly increased platelet membrane microviscosity (P = 0.02; 6 patients). Four patients, who underwent 12 months of evaluation, showed modest cognitive improvement on psychometric testing (Mini-Mental State Examination and the cognitive portion of the Alzheimer's Disease Assessment scale scores). Conclusions. While earlier literature promoted the use of zinc in AD patients, a recent study has contradicted this and implicated zinc in the aetiology of Alzheimer's disease. On the basis of the above results, it may be premature to single out zinc as a causal agent in AD.

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