Document Detail


Effect of glycolic acid on UVB-induced skin damage and inflammation in guinea pigs.
MedLine Citation:
PMID:  12218285     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: Recently the use of glycolic-acid-containing cosmetics has received increased public interest in their supposed ability to reduce wrinkles, roughness, age spots and other skin damage. However, the safety of such products when used excessively or chronically, especially by photosensitive people, is being questioned. The purpose of this study was to examine the effects of glycolic acid alone or in combination with UVB on skin damage and inflammatory response. METHOD: Guinea pigs were treated with glycolic acid (from 1 to 7 mg/cm(2)) alone or in combination with UVB (0.4 or 3 J/cm(2)) for 14 days. Skin damage was evaluated by scoring the skin irritation value by the method of Draize and by histopathological observations. Cyclooxygenase 2 (COX-2) expression and prostaglandin E(2) (PGE(2)) production were also assessed. RESULTS: Glycolic acid caused an increase in the level of skin damage in a dose- and time-dependent manner. Lower doses (1 and 3 mg/cm(2)) of glycolic acid mostly caused erythema and eschar, and these consequently formed scales, whereas higher doses (5 and 7 mg/cm(2)) of glycolic acid caused redness, edema and necrotic ulceration. Glycolic acid also increased the thickness of the epidermal layer, reduced the organization of the stratum corneum and eventually destroyed some parts of the epidermal layer at 7 mg/cm(2). UVB (0.4 and 3 J/cm(2)) caused redness and edema as well as reduced the integrity of the stratum corneum. Glycolic acid enhanced the UVB-induced skin damage. The magnitude of the damage caused by combined UVB and glycolic acid treatment was much greater than that caused by glycolic acid or UVB alone. Moreover, partial destruction of the epidermal layer was observed in skin treated with 3 J/cm(2) UVB and 3 mg/cm(2) glycolic acid. However, glycolic acid did not change the basal and UVB-induced PGE(2) production and COX-2 protein expression. CONCLUSION: These results show that glycolic acid causes skin damage in a dose- and time-dependent manner and that it enhances UVB-induced skin damage without accompanying PGE(2) production or COX-2 protein expression. Therefore, caution should be exercised by those using glycolic acid on a chronic basis or excessively. Moreover, those with photosensitive skins and those more exposed to the sun should be particularly careful.
Authors:
K S Park; H J Kim; E J Kim; K T Nam; J H Oh; C W Song; H K Jung; D J Kim; Y W Yun; H S Kim; S Y Chung; D H Cho; B Y Kim; J T Hong
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Skin pharmacology and applied skin physiology     Volume:  15     ISSN:  1422-2868     ISO Abbreviation:  Skin Pharmacol. Appl. Skin Physiol.     Publication Date:    2002 Jul-Aug
Date Detail:
Created Date:  2002-09-09     Completed Date:  2002-10-21     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9807277     Medline TA:  Skin Pharmacol Appl Skin Physiol     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  236-45     Citation Subset:  IM    
Copyright Information:
Copyright 2002 S. Karger AG, Basel
Affiliation:
Department of General Toxicology, National Institute of Toxicological Research, Korea Food and Drug Administration, Seoul, Korea.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cyclooxygenase 2
Dermis / pathology
Dinoprostone / biosynthesis
Epidermis / pathology
Female
Glycolates / adverse effects*
Guinea Pigs
Inflammation / etiology
Isoenzymes / metabolism
Keratolytic Agents / adverse effects*
Prostaglandin-Endoperoxide Synthases / metabolism
Skin / drug effects*,  metabolism,  pathology,  radiation effects*
Time Factors
Ultraviolet Rays / adverse effects
Chemical
Reg. No./Substance:
0/Glycolates; 0/Isoenzymes; 0/Keratolytic Agents; 363-24-6/Dinoprostone; 79-14-1/glycolic acid; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases

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