Latest Research on Lipid Peroxidation: Jan – 2020

Microsomal lipid peroxidation

This chapter discusses microsomal lipid peroxidation. Lipid peroxidation may be a complex process known to occur in both plants and animals. It involves the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of the double bonds in unsaturated lipids, and therefore the eventual destruction of membrane lipids, producing a spread of breakdown products, including alcohols, ketones, aldehydes, and ethers. Biological membranes are often rich in unsaturated fatty acids and bathed in an oxygen-rich, metal-containing fluid. Lipid peroxidation begins with the abstraction of a atom from an unsaturated carboxylic acid , leading to the formation of a lipid radical. The formation of lipid endoperoxides in unsaturated fatty acids containing a minimum of 3 methylene interrupted double bonds can cause the formation of malondialdehyde as a breakdown product. [1]

Lipid peroxidation and tissue damage.

In recent years it’s become apparent that the oxidation of lipids, or lipid peroxidation, may be a crucial step within the pathogenesis of several disease states in adult and infant patients. Lipid peroxidation may be a process generated naturally in small amounts within the body, mainly by the effect of several reactive oxygen species (hydroxyl radical, peroxide etc.). It also can be generated by the action of several phagocytes. These reactive oxygen species readily attack the polyunsaturated carboxylic acid s of the fatty acid membrane, initiating a self-propagating chain reaction. The destruction of membrane lipids and therefore the end-products of such lipid peroxidation reactions are especially dangerous for the viability of cells, even tissues. Enzymatic (catalase, superoxide dismutasse) and nonenzymatic (vitamins A and E) natural antioxidant defence mechanisms exist; however, these mechanisms could also be overcome, causing lipid peroxidation to require place. [2]

Lipid peroxidation: its mechanism, measurement, and significance

An increased concentration of end products of lipid peroxidation is that the evidence most often quoted for the involvement of free radicals in human disease. However, it’s likely that increased oxidative damage occurs in most, if not all, human diseases and plays a big pathological role in just a number of them. for instance , peroxidation appears to be important in atherosclerosis and in worsening the initial tissue injury caused by ischemic or traumatic brain damage. Oxidative stress can damage many biological molecules; indeed, proteins and DNA are often more significant targets of injury than are lipids, and lipid peroxidation often occurs late within the injury process. Many assays are available to live lipid peroxidation, but no single assay is an accurate measure of the entire process. Application of straightforward diene-conjugate and thiobarbituric acid (TBA) assays to human tissues and body fluids can produce artifacts. An HPLC-based TBA test can eliminate a number of these artifacts. [3]

Lipid Peroxidation in Newborn Rabbits: Effects of Oxygen, Lipid Emulsion, and Vitamin E

The extent of in vivo lipid peroxidation and therefore the in vivo antioxidant effects of α-tocopherol and α-tocopheryl acetate were studied in newborn rabbits exposed to at least one of two oxidant stresses: hyperoxia (Fio2 0.9) or parenteral lipid emulsion infusion. Lipid peroxidation was monitored by measurement of expired ethane and pentane, tissue thiobarbituric acid (TBA) reactants, and tissue lipid peroxides. Seventy-two h of hyperoxia didn’t increase any of the parameters of lipid peroxidation although mortality was higher in oxygen exposed animals. α-Tocopherol (100 mg/kg, intravenous) lowered expired hydrocarbons and tissue TBA reactants, but raised liver lipid peroxides in both air and hyperoxia exposed pups. Infusion of soyabean oil emulsion increased production of ethane and pentane, liver TBA reactants, and lung lipid peroxides. [4]

Salivary Lipid Peroxidation and Antioxidant Status in Nigerian Cigarette Smokers with or Without Periodontitis

Aim: to supply information on the susceptibility of cigarette smokers to oral diseases. This was achieved by assessing the degree of salivary oxidative stress markers in smokers with or without periodontitis. We measured salivary concentrations of malondialdehyde (MDA) and peroxide (H2O2), myeloperoxidase (MPx) activity, enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and peroxidase (GPx activities) and reduced glutathione (GSH) concentration. [5]

Reference

[1] Buege, J.A. and Aust, S.D., 1978. [30] Microsomal lipid peroxidation. In Methods in enzymology. (Web Link)

[2] Mylonas, C. and Kouretas, D., 1999. Lipid peroxidation and tissue damage. In vivo (Athens, Greece), 13(3), (Web Link)

[3] Halliwell, B. and Chirico, S., 1993. Lipid peroxidation: its mechanism, measurement, and significance. The American journal of clinical nutrition, 57(5), (Web Link)

[4] Lipid Peroxidation in Newborn Rabbits: Effects of Oxygen, Lipid Emulsion, and Vitamin E
Jon R Wispe, Matthew Knight & Robert J Roberts
Pediatric Research volume 20, (Web Link)

[5] M. Kosoko, A., A. Olayanju, O., K. Rahamon, S. and G. Arinola, O. (2017) “Salivary Lipid Peroxidation and Antioxidant Status in Nigerian Cigarette Smokers with or Without Periodontitis”, Asian Journal of Medicine and Health, 3(3), (Web Link)

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