ANALYSIS OF DL--TOCOPHEROL AS ANTIOXIDANT ON MALONDIALDEHYDE LEVEL IN PEDIATRIC PATIENTS WITH -THALASSEMIA MAJOR
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Abstract:
Thalassemia is a hereditary form of anemia that affects the synthesis of hemoglobin. The management of therapy in patients with b-thalassemia major which patients should receive continuous blood transfusions and increased iron absorption from the digestive tract causes excess iron in the body. This will lead to an increase of free iron level that triggers Radical Oxygen Species (ROS). Increased level of ROS can initiate lipid peroxidation which used as an indicator of oxidative stress in cells and tissues and produce reactive carbonyl, mainly malondialdehyde (MDA). Thus, MDA measurement is widely used as an indicator of lipid peroxidation. On the other hand, the risk of oxidative damage can be reduced by antioxidant, one of them is Vitamin E that is a fat-soluble vitamin with high potential antioxidant. The objective of this study was to analyze the effect of the dl-a-tocopherol (Vitamin E) administration on decrease of MDA serum level on pediatric patients with b-thalassemia major. This was a longitudinal observational study design for one group without comparison was conducted to examine the use of vitamin E to decreased MDA serum level on children patients with b-thalassemia major. The inclusion criteria were patients who rely on blood transfusions, patients who received only one type of iron chelating agents during the study period, the clinical condition is stable, agrees, and has completed the informed consent. In the course of the study of 21 patients there were variations in patient compliance in taking vitamin E tablet dosage 200 IU once-daily for one month: only 11 out of 21 patients consumed 30 tablets of vitamin E 200 IU (total dose of 6000 IU) in the 1-month study, and only data from those 11 samples will be analysed further. MDA serum level was measured pre- and post-administration of vitamin E and patient’s characteristics of subjects was obtained for additional information. Pre-administration of vitamin E, serum level of MDA was 1239.4 ± 502.55 ng/mL with a range of 216.95 to 2297.3 ng/mL, whereas in the group post administration of vitamin E, MDA serum level was 786.49 ± 704.88 ng/mL with a range of 6.5380 to 1958.6 ng/mL. In conclusion, there was no significant difference in MDA serum level in the group pre- and post- administration of vitamin E (p = 0.15).Keywords:
Malondialdehyde
Lipid peroxidation (LP) is determined by quantifying the malondialdehyde (MDA) content in the homogenate supernatant in the caudal adjacent segment to epicenter by colorimetric reaction with thiobarbituric acid (TBA) at high temperatures. Malondialdehyde is the principal and most studied product of polyunsaturated fatty acid peroxidation.
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Introduction: Lipid peroxidation, one of the known indices of oxidative stress, is documented in various diseases. Secondary oxidation products such as malondialdehyde (MDA) is commonly measured to observe lipid peroxidation. In this study, a spectrophotometric method was evaluated to measure thiobarbituric acid reactive substances (TBARS) with high sensitivity. This study was aimed to optimisation standard of MDA using tetraethoxypropane (TEP) 97% (FW=220.3). Methods: The method is based upon the reaction of malondialdehyde (MDA) and TBA in the glacial acetic acid medium. MDA is a known biomarker of oxidative status in a biological system. This research consists of two phases: first, making a stock of TEP, and the second phase was testing the concentration of TEP for finding the standard curve of MDA before used in diagnostic of lipid peroxidation. Results: Result showed the concentration 1,875-60 uM of TEP could form a precise standard curve. Conclusion: This concentration of TEP can be used as a reference as the standard of control in diagnostic of lipid peroxidation using TBARS method.
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It has been well-established that malondialdehyde (MDA), which is generated during the process of lipid peroxidation, is a commonly known biomarker for oxidative stress. Therefore, the serum levels of MDA are detected by using the lipid peroxidation assay with commercially available kit to determine the induction of oxidative stress in rat models.
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Lipid peroxidation products like malondialdehyde, 4-hydroxynonenal and F2-isoprostanes are widely used as markers of oxidative stress in vitro and in vivo. This study reports the results of a multi-laboratory validation study by COST Action B35 to assess inter-laboratory and intra-laboratory variation in the measurement of lipid peroxidation. Human plasma samples were exposed to UVA irradiation at different doses (0, 15 J, 20 J), encoded and shipped to 15 laboratories, where analyses of malondialdehyde, 4-hydroxynonenal and isoprostanes were conducted. The results demonstrate a low within-day-variation and a good correlation of results observed on two different days. However, high coefficients of variation were observed between the laboratories. Malondialdehyde determined by HPLC was found to be the most sensitive and reproducible lipid peroxidation product in plasma upon UVA treatment. It is concluded that measurement of malondialdehyde by HPLC has good analytical validity for inter-laboratory studies on lipid peroxidation in human EDTA-plasma samples, although it is acknowledged that this may not translate to biological validity.
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To the Editor. —In the AugustArchives(1981;141:1169-1171), Yasaka et al reported an increase in lipid peroxidation (as measured by serum malondialdehyde levels) after ingestion of paraquat, a bipyridinium compound widely used as a herbicide. The authors suggested that the serum malondialdehyde may have originated from passage of the blood through the lung or, possibly, from the liver, which has the capacity to generate reactive oxygen species in response to paraquat. In addition, it was suggested that levels of serum malondialdehyde might provide a useful indicator of the efficacy of therapeutic modalities involving free radical scavenging agents. The accompanying editorial by Fairshter (1981;141:1121-1122) addressed some of the difficulties inherent in studies involving activated oxygen species, lipid peroxidation, and the use of the malondialdehyde level as an end point of lipid peroxidation. However, several additional aspects of this initial report deserve comment in order that subsequent research be more meaningful. First,
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Free radicals generate the lipid peroxidation process in an organism. Malondialdehyde (MDA) is one of the final products of polyunsaturated fatty acids peroxidation in the cells. An increase in free radicals causes overproduction of MDA. Malondialdehyde level is commonly known as a marker of oxidative stress and the antioxidant status in cancerous patients.
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Free radicals induce lipid peroxidation, playing an important role in pathological processes. The injury mediated by free radicals can be measured by conjugated dienes, malondialdehyde, 4-hydroxynonenal, and others. However, malondialdehyde has been pointed out as the main product to evaluate lipid peroxidation. Most assays determine malondialdehyde by its reaction with thiobarbituric acid, which can be measured by indirect (spectrometry) and direct methodologies (chromatography). Though there is some controversy among the methodologies, the selective HPLC-based assays provide a more reliable lipid peroxidation measure. This review describes significant aspects about MDA determination, its importance in pathologies and biological samples treatment.
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To investigate the role of lipid peroxidation in diabetic cataractogenesis, malondialdehyde, a breakdown product of lipid peroxidation, was measured in lenses with incipient opacities and in retinas from diabetic rats and in clear lenses and in retinas from normal rats. The malondialdehyde mean values obtained in the transparent and cataractous lenses showed non-significant differences, while non-diabetic rat retinas had a significantly lower mean level of malondialdehyde compared with diabetic rat retinas (p less than 0.01). This indicates that, in streptozotocin-induced diabetic rats, lipid peroxidation is apparently not involved in the development of cataract, but it is quite probably involved in retinal damage. The retina, richer in polyunsaturated fatty acids than other ocular structures, is the elective site of lipid peroxidation and from this membrane peroxidation products might probably diffuse and damage other ocular tissues.
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