Table 1.
Types/classes of HAs | Safety evaluation | Photocarcinogenesis | Mechanism of biological action |
---|---|---|---|
αHAs | Not mutagenic or carcinogenic, not reproductive or developmental toxins, not skin sensitizers11 | No alteration of photocarcinogenesis induced by SSR13 | Reduced Ca ion concentration in the epidermis disrupts cellular adhesions by removing Ca ions from the cell adhesions by chelation allowing for exfoliation; promoting cell growth and retarding cell differentiation19 |
Glycolic acid | Increased SSR sensitivity in human skin9,10 Increased epidermal thickness, epidermal and dermal levels of hyaluronic acid, and collagen gene expression23 |
Increased epidermal proliferation in mice14 | Acceleration of collagen synthesis by fibroblasts and also modulation of matrix degradation and collagen synthesis through keratinocyte-released cytokines22 Accelerated epidermal turnover and inhibition of melanin formation in melanocytes by directly inhibiting tyrosinase activity34 Pretreatment increased UV-induced pigmentation35 |
PHA | Photoprotective (gluconolactone)33 | Function as a chelating agent and exhibits potency in scavenging free radicals33 | |
βHA | – | – | – |
SA | Enhances percutaneous penetration, not a photosensitizer, not phototoxic, no change in SSR sensitivity in human skin9 UV effects on skin sensitivity should be considered due to its keratolytic action on human skin12 |
Photoprotective, reducing the carcinogenicity of SSR13,24 Increased epidermal proliferation and thickness in mice14 |
Acts at the level of transcription to downregulate the production of fibrinogen, fibronectin, and α-hemolysin virulence factors necessary for bacterial replication in host tissues28 |