Abstract
The present study investigated the photoprotective properties of an ethanol extract derived from the red alga Bonnemaisonia hamifera against ultraviolet B (UVB)-induced cell damage in human HaCaT keratinocytes. The Bonnemaisonia hamifera ethanol extract (BHE) scavenged the superoxide anion generated by the xanthine/xanthine oxidase system and the hydroxyl radical generated by the Fenton reaction (FeSO4 + H2O2), both of which were detected by using electron spin resonance spectrometry. In addition, BHE exhibited scavenging activity against the 1,1-diphenyl-2-picrylhydrazyl radical and intracellular reactive oxygen species (ROS) that were induced by either hydrogen peroxide or UVB radiation. BHE reduced UVB-induced apoptosis, as shown by decreased apoptotic body formation and DNA fragmentation. BHE also attenuated DNA damage and the elevated levels of 8-isoprostane and protein carbonyls resulting from UVB-mediated oxidative stress. Furthermore, BHE absorbed electromagnetic radiation in the UVB range (280–320 nm). These results suggest that BHE protects human HaCaT keratinocytes against UVB-induced oxidative damage by scavenging ROS and absorbing UVB photons, thereby reducing injury to cellular components.
Highlights
Ultraviolet (UV) radiation comprises UVA, ultraviolet B (UVB) and UVC rays and causes various health problems
100 μg/mL, 13% at 150 μg/mL, and 18% at 200 μg/mL, compared with 90% for 2 mM of N-acetyl cysteine (NAC), a well-known reactive oxygen species (ROS) scavenger that was used as the positive control (Figure 1a, black bars)
We evaluated the ability of Bonnemaisonia hamifera ethanol extract (BHE) to scavenge intracellular ROS
Summary
Ultraviolet (UV) radiation comprises UVA, UVB and UVC rays and causes various health problems. UVB rays (280–320 nm) are damaging to the basal cell layer of the epidermis. UVA and UVB rays stimulate the production of reactive oxygen species (ROS) in epidermal cells, resulting in skin lesions, accelerated aging [1] and the development of malignant skin diseases [2,3,4]. When ROS are produced in excess, cellular antioxidant defense mechanisms become overwhelmed, culminating in a cascade of ROS generation that eventually results in oxidative stress. Exposure of human keratinocytes to UVB radiation leads to the immediate generation of the superoxide anion [5]. The superoxide anion can be converted into other ROS and free radicals, which have harmful effects on the skin, such as hydrogen peroxide and the hydroxyl radical [6]
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