AHAs are organic acids with one hydroxyl group attached to the alpha position of the acid. AHAs including glycolic acid, lactic acid, malic acid, tartaric acid, and citric acid are often used extensively in cosmetic formulations. AHAs have been used as superficial peeling agents as well as to ameliorate the appearance of keratoses and acne in dermatology. However, caution should be exercised in relation to certain adverse reactions among patients using products with AHAs, including swelling, burning, and pruritus.

AHAs are found throughout nature in sugarcane (glycolic acid), sour milk (lactic acid), and fruits (citric acid and malic acid). AHAs used in dermatologic and cosmetic products are usually synthetically produced. Vorarat et al. and Parker et al. have reported that AHAs could be separated in complex mixtures from fruits using capillary electrophoresis and through direct UV detection at 200 nm [18]. Therefore, obtaining a signal and determining compound purity are feasible. AHAs are small polar molecules and will disrupt the cohesion of corneocytes of the skin barrier [19], but their dermal absorption remains obscure. According to many studies, the effectiveness of AHAs is dependent on pH, concentration, and exposure time [18]. For example, AHAs are one of the ingredients for cleaning products. AHAs in rinse-off shampoos and conditioners are almost entirely removed from the skin within minutes by rinsing, resulting in an application that is extensive and fast. In chemical peeling, AHAs are used in exposure time intervals such as 35% (4 min), 52.5% (3 min), 70% (2 min) at varying intervals for up to 6 months [20]. The preceding research provide evidence that the effectiveness of AHAs is dependent on exposure time.

Over the preceding two decades, many studies have investigated the biological function and clinical application of AHAs, and results have indicated that the effectiveness of AHAs is determined by concentration and exposure time. Some clinical studies have examined the effects of topically applied GA on markers for UV-light-induced damage. UVB (280–320 nm)-induced DNA damage plays a key role in the initiation phase of skin cancer. Apoptosis and efficient repair mechanisms of DNA damage protect human keratinocytes against UVB [21]. One study determined that that topical application of 10% GA for 12 weeks increased the sensitivity of the skin to UV light and enhanced the formation of sunburn cells (SBCs) [7]. Our previous study demonstrated that cotreatment of AHAs with a high concentration of GA (5 mM) and UVB had a synergistic effect on apoptosis in human keratinocyte HaCaT cells [9]. The results of these studies suggest that the use of AHA substances on the skin requires caution.