1997
DOI: 10.1016/s0005-2760(97)00093-3
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Oxidative damage of human skin lipids

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Cited by 29 publications
(12 citation statements)
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“…39 The sebaceous gland releases sebum through the follicular duct to the uppermost skin layer, where several factors can induce the lipid oxidation including Propionibacterium acnes, UV exposure, or natural ROS. [40][41][42][43][44] The present findings and the previous studies suggest that skin lipids become more sensitive to the oxidation process than the body adipose tissue as hamsters grow older.…”
Section: Chemometrics Analysissupporting
confidence: 79%
“…39 The sebaceous gland releases sebum through the follicular duct to the uppermost skin layer, where several factors can induce the lipid oxidation including Propionibacterium acnes, UV exposure, or natural ROS. [40][41][42][43][44] The present findings and the previous studies suggest that skin lipids become more sensitive to the oxidation process than the body adipose tissue as hamsters grow older.…”
Section: Chemometrics Analysissupporting
confidence: 79%
“…644 A study of the oxidative damage to human skin lipids shows that peroxidation of fatty acids depended on the concentration of cholesterol. 645 The rate of lipid peroxidation of n-3 polyunsaturated fatty acids was found not to be suppressed by vitamin E ( -tocopherol) supplementation in the diet. 646 The loss of fluorescence of cis-parinaric acid [18:4(9Z,11Z,13Z,15Z)] is a sensitive indicator of lipid peroxidation, which has been applied to the study of peroxidation of unsaturated fatty acids in immune cells.…”
Section: Lipid Peroxidation and Autoxidationmentioning
confidence: 95%
“…The origins of radical initiators are oxidative environmental exposures and possibly also naturally occurring cutaneous bacteria which are a newly suggested source of oxidative entities (see below). Lipid peroxidation is a physiological process occurring naturally in the skin, but is nonetheless a chain reaction which can be deleterious to the cells and is often difficult to control, while its end products may interfere with normal cellular functions, affecting the delicate cutaneous PR homeostasis [ 59 ]. It is well established that α,β-unsaturated aldehydes (which are also ALEs) are able to activate the Nrf2–Keap1 pathway by direct Keap1 oxidation [ 52 , 60 ].…”
Section: Skin- and Bacteria-derived Metabolites Affect Pr Homeostamentioning
confidence: 99%