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60 SKINCARE


contributing to a variety of medical disorders. These include atherosclerosis, Alzheimer’s disease, heart failure, rheumatoid arthritis, and cancer. They are harmful to cell membranes, cause DNA mutations, damage proteins, and can alter the synthesis rates of enzymes, cytokines, and other molecules. If unchecked, these effects can cause a


variety of pathologies, both acute and chronic, including cell death. Circulating proteins and lipoproteins modified by lipid peroxidation can also stimulate the formation of antibodies.


Lipid peroxides, sunlight, and photo- ageing The surface lipids of skin are derived from epithelial cells and sebum produced by the sebaceous glands. Their function is to reduce water loss by evaporation and provide a protective barrier against external chemicals and pathogens. The most abundant unsaturated lipids in skin are squalene, triglycerides, cholesterol, sebaleic acid (5,8-octadecadienoic acid), linoleic acid, and phospholipids. The UVA and UVB wavelengths of sunlight,


especially the former, are well known to increase the production of ROS, and consequently lipid peroxidation. There is much less awareness of the fact that the effect is not limited to the UV wavelengths. Not only do visible and infra-red radiation also produce ROS, but their combined contribution has been estimated to be similar to that of UV.1 Skin is also exposed to other agents that


increase lipid peroxidation, namely atmospheric pollutants. All of the most abundant pollutants in urban environments have been shown to promote ROS formation – nitrogen dioxide, ozone, polycyclic aromatic hydrocarbons, fine particulate matter, and tobacco smoke.2 Studies in vitro have shown that dermal


fibroblasts, keratinocytes, and extracellular proteins are all damaged by products of lipid peroxidation, especially the reactive aldehydes MDA and 4-HNE. The propagation of oxidative chain reactions among unsaturated phospholipids in the plasma (surface) membranes of cells can interfere with their functions, and if unchecked lead to cell death. The formation of covalent adducts of


MDA and 4-HNE with specific amino acids of extracellular proteins, such as collagen and elastin, can cause them to aggregate,3


the strength and elasticity of skin, while the formation of adducts with enzymes can reduce their activities. In cultured fibroblasts, lipid peroxidation products stimulate the secretion of collagenases, such as matrix metalloproteinase-1 (MMP-1),4


and in both


fibroblasts and keratinocytes they induce the synthesis of pro-inflammatory cytokines.5 These multiple effects are the cause of the thinning, dryness, wrinkles, and lentigines that occur in skin during ageing. Cumulative damage to the DNA of fibroblasts, keratinocytes, and melanocytes, considered in more detail below, are additional causes of skin ageing. The effects of lipid peroxides on cytokines are factors in the acute inflammation of sunburn, and there is experimental evidence that their effects on nerves cause the associated pain.6


PERSONAL CARE March 2023 reducing MDA p=0.01 1.0 1.0


Control ■ UV alone ■ UV plus peptide ■ 8-OHdG


p=0.001


0.5


0.5


0.0 4HNE p=0.001 1.0 1.0


0.0 IL-6 p=0.05


0.5


0.5


0.0


0.0


Figure 2: Effects of LipoxErase peptide on DNA damage (8-OHdG), MDA concentration, 4-HNE-protein adducts, and IL-6 synthesis (by qRT-PCR) in cultures of keratinocytes. UV, ultraviolet irradiation


Lipid peroxides, DNA, and skin cancer Despite increasing sales of UV screens, the incidence of skin cancers has been rising worldwide for many years at rates that cannot be fully explained by stratospheric ozone depletion.7


Like cancers in other tissues, all


types of skin cancer - malignant melanoma, squamous cell carcinoma, and basal cell carcinoma - are caused by damage to DNA. This is partly owing to a direct effect of


sunlight. But this is only part of the story. Lipid peroxidation products are also highly mutagenic. One of the most important mutations results from the formation of 8-hydroxy-deoxyguanosine (8-OHdG) as a consequence of the reaction of MDA with the nucleotide guanine.8


Lipid peroxides and acne vulgaris Acne vulgaris affects about 9% of the world population. It is a chronic disorder of the pilosebaceous units, which become distended with sebum, hyperkeratinised, and colonised with Propionibacterium acne, a commensal organism that thrives in hypoxic lipid-rich environments. The aetiology is not known. Although P. acne has attracted much


attention as a possible initiating factor, reports that the surface densities of the organism did not differ between people with and without acne, and that many inflamed lesions showed no evidence of colonization,14


different aetiology. The idea that this could be peroxidation


4-HNE can also react with


the other nucleotides of DNA, although guanine is the most common.9 These adducts of nucleotides with


aldehydes occur in both nuclear and mitochondrial DNA. The genes most commonly affected differ between the different types of skin cancer. In squamous cell carcinoma, the second most common type of skin cancer, causing about 8000 deaths per year in the USA, mutations are found most commonly in the NOTCH and p53 signalling pathways that control cell division.10 In malignant melanoma, much more serious but also the least common skin cancer, the BRAF and NRAS pathways are most commonly affected.11


In basal cell carcinoma, the most


common cancer anywhere in the body, yet other tumour suppressor and proto-oncogenes are affected.12


In the pre-cancerous lesions of


seborrheic keratosis, the most common site of DNA damage is the gene that codes for a fibroblast growth hormone receptor.13


of sebum lipids, with colonization by P. acne being a secondary opportunistic infection, has received support from several lines of evidence. Squalene is rapidly and extensively oxidised by UV radiation and atmospheric pollution, and the sebum of individuals affected by acne contains higher concentrations of squalene peroxides than that of non-affected subjects, despite similar squalene secretion rates.15 The concentrations of both lipid


peroxidation products and the inflammatory cytokine interleukin-1α were found to be higher in inflamed than in non-inflamed comedones.16 In cultures of keratinocytes, squalene peroxides increased the synthesis of the inflammatory mediator interleukin-6.17 When applied to the skin of mice,


UV-induced squalene peroxides had an immunosuppressive effect.18


When


applied to the ears of rabbits, squalene monohydroperoxide, but not squalene, caused comedones to develop that were histologically similar to those of acne, and whose size


www.personalcaremagazine.com


have suggested a


Normalized 4-HNE value


Normalized MDA value


Ratio


Normalised value


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