Abstract：
Vitamin K possesses efficacy as a topical dermatological agent. However, vitamin K is phototoxic and susceptible to photodegradation. Herein, we investigated the mechanisms underlying the phototoxicity of phylloquinone (PK, vitamin K1) and menaquinone-4 (MK-4, vitamin K2) under ultraviolet A (UVA) irradiation using various reactive oxygen species (ROS) scavengers. This resulted in the production of superoxide anion radicals via type I and singlet oxygen via type II photodynamic reactions, which were quenched by the ROS scavengers: superoxide dismutase and sodium azide (NaN3). In HaCaT cells, MK-4 and PK induced the production of intracellular ROS, particularly hydrogen peroxide, in response to UVA irradiation. Furthermore, the addition of catalase successfully decreased maximum ROS levels by approximately 30%. NaN3 and catalase decreased the maximum reduction in cell viability induced by UVA-irradiated PK and MK-4 in cell viability by approximately 2-7-fold. Additionally, ROS scavengers had no effect on the photodegradation of PK or MK-4 at 373 nm. Therefore, the phototoxicities of PK and MK-4 were attributed to the generation of singlet oxygen and hydrogen peroxide, underscoring the importance of photoshielding in circumventing phototoxicity.
摘要：
维生素K具有作为局部皮肤病剂的功效。然而,维生素K具有光毒性，易于光降解。在这里，我们研究了苯醌光毒性的潜在机制(PK，维生素K1）和甲基萘醌-4（MK-4，维生素K2）在紫外线A（UVA）照射下使用各种活性氧（ROS）清除剂。这导致通过I型产生超氧阴离子自由基，并通过II型光动力反应产生单线态氧，其被ROS清除剂:超氧化物歧化酶和叠氮化钠(NaN3)淬灭。在HaCaT细胞中,MK-4和PK诱导细胞内ROS的产生，特别是过氧化氢，响应UVA照射。此外，过氧化氢酶的添加成功地将最大ROS水平降低了约30%。NaN3和过氧化氢酶将UVA照射的PK和MK-4诱导的细胞活力的最大降低降低约2-7倍。此外,ROS清除剂对PK或MK-4在373nm处的光降解没有影响。因此,PK和MK-4的光毒性归因于单线态氧和过氧化氢的产生，强调光屏蔽在规避光毒性中的重要性。
