Abstract
Exposure to UV solar radiation is important for human health and well-being, but is also the cause of photooxidative skin damage resulting in sunburn, photoaging and skin cancer. Marine microalgae are a natural source of photoprotective compounds that, based on their UV light absorbing and strong antioxidant properties, have the potential for use in sun protection and health care products. In this thesis, I have investigated whether the bioactive xanthophyll, diatoxanthin, which is produced in the marine diatom Phaeodactylum tricornutum, can protect human skin from photodamage. As a model for photodamage in skin, the human immortalized keratinocyte cell line N/TERT1 was exposed to a combination of UVA and UVB radiation, before cell viability, ROS formation, and the release and gene expression of inflammatory markers were measured. The capacity of diatoxanthin to protect against photodamage was compared to a second bioactive xanthophyll, fucoxanthin, and the potent antioxidant astaxanthin. We found that the confluency of the keratinocyte cell culture affected the response to UVR, with high density differentiated cultures being less susceptible to UVR-induced cell death than proliferating cultures. Exposure to a combination of 0.76 J/cm² UVA and 0.04 J/cm² UVB radiation was sufficient to increase ROS production in N/TERT1 cells, without causing cell death. A combination of 3.8 J/cm² UVA and 0.2 J/cm² UVB radiation increased the release of the inflammatory signalling molecules TNFa and PGE2, associated with increasing gene expression. We found no cytotoxic or phototoxic effects of the microalgal pigments in the N/TERT1 cells. Incubation with 100 ng/mL diatoxanthin, 1 ng/ml astaxanthin, or 1, 100 or 500 ng/ml fucoxanthin before exposure to UVR reduced the intracellular ROS. However, we found no effect of diatoxanthin or fucoxanthin on the UVR induced release or expression of inflammatory markers. Together our findings indicate that while we observed some antioxidant effects of diatoxanthin in the normal keratinocyte model, this was not sufficient to suppress the pro-inflammatory effects of UVR.