Protective effect of melatonin on ascorbate‐Fe<sup>2+</sup> lipid peroxidation of polyunsaturated fatty acids in rat liver, kidney and brain microsomes: a chemiluminescence study

Leaden, Patricio; Catalá, Ángel

doi:10.1111/j.1600-079x.2005.00232.x

Cited by 15 publications

(11 citation statements)

References 25 publications

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“…They showed that fatty acid composition of total lipids isolated from rat liver microsomes was substantially modified when subjected to nonenzymatic lipid peroxidation with a considerable decrease of both n-3 and n-6 polyunsaturated fatty acids (PUFA) Table 1. It was considered that melatonin may act in vivo and in vitro as an antioxidant protecting long chain PUFA present in rat liver microsomes from the deleterious effect by a selective mechanism that reduces the loss of docosahexaenoic acid (DHA, 22:6 n-3) and arachidonic acid (AA, 20:4 n-6) [13,51].…”

Section: Melatonin Prevents Polyunsaturated Fatty Acid Peroxidation Imentioning

confidence: 99%

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The Ability of Melatonin to Counteract Lipid Peroxidation in Biological Membranes

Catalá

2007

CMM

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This paper reviews recent data relevant to the antioxidant effects of melatonin with special emphasis on the changes produced in polyunsaturated fatty acids located in the phospholipids of biological membranes. The onset of lipid peroxidation within cellular membranes is associated with changes in their physicochemical properties and with the impairment of protein functions located in the membrane environment. All cellular membranes are especially vulnerable to oxidation due to their high concentration of polyunsaturated fatty acids. These processes combine to produce changes in the biophysical properties of membranes that can have profound effects on the activity of membrane-bound proteins. This review deals with aspects for lipid peroxidation of biological membranes in general, but with some emphasis on changes of polyunsaturated fatty acids, which arise most prominently in membranes and have been studied extensively in our laboratory. The article provides current information on the effect of melatonin on biological membranes, changes in fluidity, fatty acid composition and lipid-protein modifications during the lipid peroxidation process of photoreceptor membranes and modulation of gene expression by the hormone and its preventive effects on adriamycin-induced lipid peroxidation in rat liver. Simple model systems have often been employed to measure the activity of antioxidants. Although such studies are important and essential to understand the mechanisms and kinetics of antioxidant action, it should be noted that the results of simple in vitro model experiments cannot be directly extrapolated to in vivo systems. For example, the antioxidant capacity of melatonin, one of the important physiological lipophilic antioxidants, in solution of pure triglycerides enriched in omega-3 polyunsaturated fatty acids is considerably different from that in subcellular membranes.

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Section: Melatonin Prevents Polyunsaturated Fatty Acid Peroxidation Imentioning

confidence: 99%

“…Statistically significant differences between samples peroxidized with and without melatonin are indicated by *P < 0.05. FromLeaden & Catalá, 2005.…”

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confidence: 99%

The Ability of Melatonin to Counteract Lipid Peroxidation in Biological Membranes

Catalá

2007

CMM

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“…All operations were carried out at 4 °C [9] . Lipid peroxidation of microsomes was measured as described previously [17] with the following modifications: the membranes, at a concentration of 1.5 mg protein, were incubated at 37 °C with 0.05 mol/L phosphate (pH 7.4) and 0.4 mmol/L ascorbic acid. The final volume was 1.5 mL.…”

Section: Methodsmentioning

confidence: 99%

Prevention of lipopolysaccharide-induced injury by 3,5-dicaffeoylquinic acid in endothelial cells

Zha

Wang

et al. 2007

Acta Pharmacologica Sinica

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Aim: To investigate the effect of 3,5-dicaffeoylquinic acid (3,5-diCQA) on lipopolysaccharide (LPS)-induced injury in human dermal microvascular endothelial cells (HMEC-1). Methods: The anti-oxidant effect was detected using the malondialdehyde (MDA) assay in a rat liver microsome model of lipid peroxidation. Cell viability was analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide assay. Cell lipid peroxide injury was measured by lactate dehydrogenase (LDH) release. Apoptotic cells were detected by flow cytometry, and confirmed by DNA fragmentation analysis. Caspase-3 activity was measured using a specific assay kit. The level of intracellular reactive oxygen species (ROS) was determined by flow cytometry with a 2,7-dichlorodihydrofluorescein diacetate fluorescence probe. Results: The exposure of microsomes to ascorbate-Fe 2+ resulted in lipoperoxidation according to an increase in the level of MDA. MDA formation decreased in a dose-dependent manner on treatment with 5, 10, or 50 µmol/L 3,5-diCQA. Treatment with LPS for 16 h resulted in a 60% decrease in cell viability and an increase in LDH release from 47.6% to 61.5%. DNA laddering was observed by agarose gel electrophoresis. The level of apoptotic cells peaked at 27% after treatment with LPS for 12 h. Following treatment with LPS for 12 h, intracellular ROS and caspase-3 activity increased. Pretreatment with 3,5-diCQA at 5, 10, or 50 µmol/L for 1 h attenuated LPS-mediated endothelial cell injury. The anti-apoptotic action of 3,5-diCQA was partially dependent on its capacity for anti-oxidation and the suppression of caspase-3 activity. Conclusion: 3,5-diCQA displays anti-oxidative and anti-apoptotic activity in HMEC-1 due to scavenging of intracellular ROS induced by LPS, and the suppression of caspase-3 activity.

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“…In addition, melatonin is an efficient scavenger of the primary hydroxyl radical. Research results indicate that a selective protection of C20:4n6 and C22:6n3 by melatonin occurs during non-enzymatic lipid peroxidation of rat liver, kidney, and brain microsomes [49]. Due to the multiple effects of melatonin, this hormone may likely exert its actions through multiple mechanisms, and a more determined approach to the study of melatonin as an anti-aging factor is warranted.…”

Section: Melatonin and Other Regulators Of Radical-dependent Reactionsmentioning

confidence: 97%

Biological Membranes Are Nanostructures that Require Internal Heat and Imaginary Temperature as New, Unique Physiological Parameters Related to Biological Catalysts

2010

Cell Biochem Biophys

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In 1961, Peter Mitchell advanced a new idea for solving the problem of coupling between oxidation and phosphorylation, but some aspects of the relationship between the redox-chain as a potential energy donor and different energy acceptors remain largely unknown. The main structure-function relationships behind catalytic rate optimization in membrane enzymes are highly important, and comparative analyses of the energetics of catalytic reactions from membrane proteins of different destination are needed to advance our understanding. Moreover, the mode of control of primary radicals, such as reactive oxygen species (ROS), should be considered. For example, iron is essential for most organisms because it serves as an electron donor and acceptor in various metabolic processes. However, these chemical properties also allow iron to participate in the formation of ROS that cause substantial damage to lipids; iron can contribute to excess production of damaging ROS through Fenton chemistry. The evidence that iron contributes to various diseases of ageing is to be examined along with the need for low or moderate levels of iron, depending on homeostasis level. If this level in the organs and tissues is close to the optimal amount needed for an initiation of lipid-radical cycles, which may be responsible for the effectiveness of some membrane enzymes, this might minimize the ROS production and retard the processes related to ageing. To my mind, biological membranes possess an internal heat and imaginary temperature that are new, unique physiological parameters related to a role as factors of biological catalysis. This is speculation and additional studies will be needed to determine whether the imaginary temperature has an equal importance with the real temperature in cellular metabolism, membrane energetics (microsomal monooxygenase and ATP synthesis) and ageing.

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Protective effect of melatonin on ascorbate‐Fe²⁺ lipid peroxidation of polyunsaturated fatty acids in rat liver, kidney and brain microsomes: a chemiluminescence study

Cited by 15 publications

References 25 publications

The Ability of Melatonin to Counteract Lipid Peroxidation in Biological Membranes

The Ability of Melatonin to Counteract Lipid Peroxidation in Biological Membranes

Prevention of lipopolysaccharide-induced injury by 3,5-dicaffeoylquinic acid in endothelial cells

Biological Membranes Are Nanostructures that Require Internal Heat and Imaginary Temperature as New, Unique Physiological Parameters Related to Biological Catalysts

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Protective effect of melatonin on ascorbate‐Fe2+ lipid peroxidation of polyunsaturated fatty acids in rat liver, kidney and brain microsomes: a chemiluminescence study

Cited by 15 publications

References 25 publications

The Ability of Melatonin to Counteract Lipid Peroxidation in Biological Membranes

The Ability of Melatonin to Counteract Lipid Peroxidation in Biological Membranes

Prevention of lipopolysaccharide-induced injury by 3,5-dicaffeoylquinic acid in endothelial cells

Biological Membranes Are Nanostructures that Require Internal Heat and Imaginary Temperature as New, Unique Physiological Parameters Related to Biological Catalysts

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Protective effect of melatonin on ascorbate‐Fe²⁺ lipid peroxidation of polyunsaturated fatty acids in rat liver, kidney and brain microsomes: a chemiluminescence study