The toxicity of 2,6-dichlorobenzoquinone on the early life stage of zebrafish: A survey on the endpoints at developmental toxicity, oxidative stress, genotoxicity and cytotoxicity
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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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The study involved 53 patients with arterial hypertension in chronic kidney disease (chronic glomerulonephritis (CGN)). Lipid peroxidation was studied based on the content of diene conjugates and malondialdehyde. Protein peroxidation was studied based on the content of 2,4-dinitphenyl-aldogidrazons. The patients in all clinical variants of the CGN revealed increased activity of lipid peroxidation and the protein peroxidation, which is most pronounced in patients with nephrotic variant of CGN: increased levels of serum malondialdehyde medians occurred in 3.92 times and diene conjugates in 1.52 times (p<0.01). Increased activity of the oxidation of lipids and proteins has a negative impact on the organization of cell membranes of the renal structures and leads to loss of membrane barrier function.
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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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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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