Effect of Glycolic Acid on UVB-Induced Skin Damage and Inflammation in Guinea Pigs

Abstract

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/cm²) alone or in combination with UVB (0.4 or 3 J/cm²) 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 E₂ (PGE₂) 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/cm²) of glycolic acid mostly caused erythema and eschar, and these consequently formed scales, whereas higher doses (5 and 7 mg/cm²) 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/cm². UVB (0.4 and 3 J/cm²) 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/cm² UVB and 3 mg/cm² glycolic acid. However, glycolic acid did not change the basal and UVB-induced PGE₂ 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 PGE₂ 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.

Human skin cell stress response to GSM‐900 mobile phone signals

“…Inflammatory processes in the skin produce lesions and thickening of the epidermis [30–32]. We therefore used epidermis thickness measurements in hRE slices as a marker for inflammation.…”

Effect of chemical peeling on the skin in relation to UV irradiation

“…Park et al (16) reported that GA treatment at dosage of 1-7 mg ⁄ cm 2 (pH 3.0) once daily for 2 weeks immediately after UVB irradiation (0.4 and 3.0 J ⁄ cm 2 ) enhanced redness and oedema, however, did not change the basal and UVB-induced prostaglandin E 2 (PGE 2 ) production and cyclooxygenase-2 (COX-2) protein expression in guinea pig. Their dose of 1-7 mg ⁄ cm 2 was achieved by applying 10-70% of GA. As both the UVB and GA dose were rather high, skin damage such as destruction of the entire epidermis was observed, especially in the dosage of 5 and 7 mg ⁄ cm 2 .…”

The use of hydroxy acids on the skin: characteristics of C8‐lipohydroxy acid

“…But since early investigations related the process of exfoliation to mild wounding and inflammation, the interpretations of increased epidermal thickness and cell division were questionable. It now seems more certain that the effect of low concentrations of hydroxy acids does not evoke an inflammatory response 14–16 and indeed SA may even be anti‐inflammatory 17…”

“…In animal models, topically applied GA and SA have been found to increase epidermal cell division 13,18 and in some experiments, a wave of cell proliferation has been observed 12–16 h after topical application 19 . Several authors have reported that, in human biopsy material, hydroxy acid treatment significantly increases the thickness of basal and suprabasal layers of the epidermis, while it tended to decrease the thickness of the stratum corneum 10,14,16,18–22 . Some investigators have, however, failed to observe an increase in cell division with SA treatment 7,8,23 .…”

“…In a clinical study on humans, another clear difference between the hydroxy acids emerges from various levels of sensitivity of treated skin when exposed to UV radiation. The AHAs appear to increase skin sensitivity to UV radiation 38,39 and consequently enhance UVB‐induced skin damage 16 . In contrast, following the daily application of C8‐LHA, the skin's resistance to UV‐induced damage was increased: the minimal erythema dose raised to 210 mj/cm 2 vs. 140mj/cm 2 for both untreated and placebo‐treated controls (C. Montastier, L’Oreal Recherche, 1994, data on file).…”