Latest News on lipid peroxidation : Jun 2022

Lipid peroxidation: its mechanism, measurement, and significance

An increased concentration of end products of lipid peroxidation is the evidence most frequently quoted for the involvement of free radicals in human disease. However, it is likely that increased oxidative damage occurs in most, if not all, human diseases and plays a significant pathological role in only some of them. For example, 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 in the injury process. Many assays are available to measure lipid peroxidation, but no single assay is an accurate measure of the whole process. Application of simple diene-conjugate and thiobarbituric acid (TBA) assays to human tissues and body fluids can produce artifacts. An HPLC-based TBA test can eliminate some of these artifacts. [1]

Mechanisms of lipid peroxidation

This article provides an overview of how peroxidation of unsaturated lipids takes place and how it can be measured. Several different aspects of free-radical-mediated lipid peroxidation are discussed, including: (a) the catalytic role of chelated iron and other redox metal ions; (b) induction by reducing agents such as superoxide, ascorbate, and xenobiotic free radicals; (c) suppression by antioxidant chemicals and enzymes; and (d) how peroxidation that depends on pre-existing hydroperoxides (lipid hydroperoxide-dependent initiation of lipid peroxidation) can be distinguished from that which does not (lipid hydroperoxide-independent initiation of lipid peroxidation). Attention is also given to non-radical, singlet oxygen-driven peroxidation and how this can be resolved from radical-driven processes. [2]

Measurement of Lipid Peroxidation

Lipid peroxidation results in the formation of conjugated dienes, lipid hydroperoxides and degradation products such as alkanes, aldehydes and isoprostanes. The approach to the quantitative assessment of lipid peroxidation depends on whether the samples involve complex biological material obtained in vivo, or whether the samples involve relatively simple mixtures obtained in vituo. Samples obtained in vivo contain a large number of products which themselves may undergo metabolism. The measurement of conjugated diene formation is generally applied as a dynamic quantitation e.g. during the oxidation of LDL, and is not generally applied to samples obtained in vivo. Lipid hydroperoxides readily decompose, but can be measured directly and indirectly by a variety of techniques. The measurement of MDA by the TBAR assay is non-specific, and is generally poor when applied to biological samples. More recent assays based on the measurement of MDA or HNE-lysine adducts are likely to be more applicable to biological samples, since adducts of these reactive aldehydes are relatively stable. The discovery of the isoprostanes as lipid peroxidation products which can be measured by gas chromatography mass spectrometry or immunoassay has opened a new avenue by which to quantify lipid peroxidation in vivo, and will be discussed in detail. [3]

Radical Scavenging, Reducing Power, Lipid Peroxidation Inhibition and Chelating Properties of Extracts from Artemisia campestris L. Aerial Parts

In this study, we estimated the antioxidant activity of various extracts prepared from Artemisia campestris L. aerial parts used in Algeria to treat gastro-intestinal disorders. The determination of polyphenols and flavonoids contents showed that the ethyl acetate extract (EAE) is rich in phenolic compounds with 481.25±0.026 mg gallic acid equivalent/g dry weight, while the chloroform extract (CHE) had the highest content of flavonoid with 34.37±0.056 mg quercetin equivalent/g dry weight. The evaluation of DPPH scavenging activity of extracts confirmed that EAE is the most active extract with IC50 of 0.0058 mg/ml. In addition, EAE showed the most scavenging activity against hydroxyl radical generated in the H2O2/Fe+2 system with IC50 of 0.17 mg/ml which is comparable to the activity of the standard antioxidant ascorbic acid (0.15 mg/ml). Ferrous ion chelating capacity assay showed that aqueous extract (AQE) was the most active with 0.11 mg/ml. The inhibition of linoleic acid/ß-carotene coupled oxidation was estimated by the ß- carotene bleaching assay, which showed a highest relative antioxidant activity for the crude extract (CE) (82.72% of inhibition). In conclusion, the present study showed that EAE of A. campestris L. is rich in phenolics and flavonoids and has a considerable antioxidant activity. [4]

Total Phenolic Contents and Lipid Peroxidation Potentials of Some Tropical Antimalarial Plants

In this investigation extracts of leaves and barks from five tropical antimalarial plants namely; Magnifera indica, Anacardium occidentale, Azachiractha indica, Carica papaya Linn and Cymbopogm citrates were studied in vitro for their total phenolics, total flavonoids and inhibition of lipid peroxidation abilities. Crude extracts from each plant material were obtained by maceration in ethanol and water respectively. The FolinCiocalteu procedure was used to assess the total phenolic concentrations of the extracts and results expressed as gallic acid equivalents (GAE). Total flavonoid contents in extracts were determined by the aluminium chloride colorimetric assay and expressed as quercetin equivalents (QAE). The percentage inhibition of lipid peroxidation was assayed by estimating the thiobarbituric acid-reactive substances (TBARS). The phenolic contents in water extracts of Anacardium occidentale leaves was 452.57 ± 8.08mg/gGAE and that of bark was recorded as 267.15 ± 6.06mg/gGAE. The ethanolic and water extracts of Azachiractha indica bark were found to be 310.71 ± 7.07mg/gGAE and 390.64 ± 6.97mg/gGAE respectively. The extracts of Magnifera indica leaves had the highest flavonoid content of 139.08 ± 0.77mg/100gQAE in ethanol and 69.55 ± 0.39 mg/100gQAE in water. The least values observed were 21.19 ± 0.64 mg/100gQAE for water extract of Anacardium occidentale leaves and 30.73 ± 0.26 mg/100gQAE for ethanolic extract of Anacardium occidentale bark. Inhibition of lipid peroxidation in liver and kidney were observed as 15.92 ± 3.01% and 17.10 ± 3.48% in ethanolic extracts of Anacardium occidentale bark and leaves respectively while it was 30.67 ± 0.47% for Carica papaya Linn. The water extract of Azachiractha indica bark inhibited liver lipid peroxidation by 8.70 ± 0.32% while that of Anacardium occidentale bark inhibited kidney lipid peroxidation by 11.78 ± 1.08%. These results suggest a need for further examination of the water extract of Anacardium occidentale bark as this part of the plant appears to be critical in the phytotherapy of malaria infection. [5]


[1] Halliwell, B. and Chirico, S., 1993. Lipid peroxidation: its mechanism, measurement, and significance. The American journal of clinical nutrition, 57(5), pp.715S-725S.

[2] Girotti, A.W., 1985. Mechanisms of lipid peroxidation. Journal of free radicals in biology & medicine, 1(2), pp.87-95.

[3] Moore, K. and Roberts, L.J., 1998. Measurement of lipid peroxidation. Free radical research, 28(6), pp.659-671.

[4] Djidel, S., 2014. Radical scavenging, reducing power, lipid peroxidation inhibition and chelating properties of extracts from Artemisia campestris L. Aerial parts. Annual Research & Review in Biology, pp.1691-1702.

[5] Iyawe, H.O.T. and Azih, M.C., 2011. Total phenolic contents and lipid peroxidation potentials of some tropical antimalarial plants. European Journal of medicinal plants, pp.33-39.

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