From Fig. 3 one can observe that sunscreen A spread on glass is prone to undergo photo-oxidation as documented by the significant increase in TBARS upon UVA exposure, as previously observed (Damiani et al., 2010). This is in analogy with the photoinstability observed in the UV absorbance spectra (Fig. 1): any BMDBM not involved in cyclo-addition with OMC, can undergo cleavage leading to ROS which contribute to increasing TBARS levels following UVA exposure. Any ROS generated by photoactivation of TiO2 may also play a part in this increase (Carlotti et al., 2009). When sunscreen A was spread onto all the skin samples, an increase in TBARS was observed with respect to the non-irradiated control which was significant for pig ear skin and human SCE membranes, but not for pig SCE membranes. The increase observed is likely due to the photo-oxidation of the sunscreen as observed on the glass plates. Furthermore, any photo-products generated upon UVA exposure of the sunscreen may interact with the lipid components of the skin samples which could also contribute to increasing the TBARS levels. However, the TBARS assay cannot discriminate between break-down products of lipid peroxidation deriving from the sunscreen and those deriving from the skin samples. Despite this, of note is the fact that increased TBARS can be detected from UVA + sunscreen exposed skin when a photounstable sunscreen is used, despite the fact that all sunscreens nowadays contain antioxidants. This is undesirable because not only is the photoprotective efficiency of the sunscreen reduced, but also photo-induced lipid peroxidation in the sunscreen may lead to potentially toxic breakdown products which remain on the skin for as long as the sunscreen is present. At worst, they may interact with skin components and/or with other co-formulated sunscreen ingredients.