Involvement of Type‐I and Type‐II Photodynamic Reactions in Photosensitization of Fragrance Ingredient 2‐acetonaphthone. (10th February 2022) - Chandra, Sonam
ABSTRACT: 2‐Acetonaphthone (2‐ACN) is a synthetic fragrance material used in various cosmetics as an adulterant. Due to its frequent use, we have conducted an in‐depth study to understand the photosensitizing potential of 2‐ACN. Results of this study illustrate that 2‐ACN showed photodegradation in 4 h under ambient UV radiation (UVR) and sunlight exposure. It generated (1–25 µg mL −1 ) superoxide anion radical (O2 · – ) and singlet oxygen ( 1 O2 ) in the presence of UVR/sunlight through in chemico and in vitro test systems. 2‐ACN (10 µg mL −1 ) showed a 43.9% and 57.4% reduction in cell viability under UVA and sunlight, respectively. Photosensitized 2‐ACN generated intracellular reactive oxygen species (ROS) (6‐folds in UVA and 8‐folds in sunlight), which compromises the endoplasmic reticulum and mitochondrial membrane potential leading to cell death. Acridine orange/ethidium bromide dual staining and annexin‐V/PI uptake showed cell death caused via 2‐ACN under UVR exposure. The above findings signify the role of ROS via Type‐I and Type‐II photodynamic pathways in photosensitization of 2‐ACN that ultimately promotes photodamage of important cellular organelles leading to cell death. The study advocates that solar radiation should be avoided by the users after the application of cosmetic products containing 2‐ACN. Abstract : The schematic representation shows the effect of 2‐ACN photosensitized by UVR and sunlight exposure. Photosensitized 2‐ACN showing photodegradation and generating singlet ( 1 O2 ) and superoxide anion radicals (O2 · – ) via Type‐I and Type‐II photodynamic reactions. Photosensitized 2‐ACN elevates the intracellular ROS level, compromising mitochondrial and endoplasmic reticulum membrane leading to Ca 2+ release in the cytosol. Excessive ROS causes an increase in cytosolic Ca 2+ and a decline in MMP leading to apoptosis and necrosis in the cells. These subcellular damages ultimately cause cell death.