DNA Damage Photoinduced by Cosmetic Pigments and Sunscreen Agents under Solar Exposure and Artificial UV Illumination

Abstract

Nanostructured ZnO particles present in skin-care cosmetics and UVB/UVA sunscreen products generate strong oxidizing species (free radicals) when illuminated with UV radiation that can damages human skin and the horny layer. Damage to DNA by ZnO and other pigmentary ingredients in sunscreen formulations under artificial and solar UV exposure has been examined by Agarose gel electrophoresis using pUC 18 DNA plasmids (2686 base-pairs). Initial photoinduced oxidative damage done to DNA plasmids have been probed by nicking assays under in vitro conditions for ZnO. The effects of nanosize ZnO and CeO 2 particles, and the newly developed CaO-doped and SiO 2-coated CeO 2 pigment are compared when subjected to artificial (75-W Hg-lamp) and solar UV radiation. Supercoiled DNA plasmids undergo one nick to produce the relaxed form, followed by a second nick yielding the linear form of the plasmids. The DNA constituents deoxyadenosine-5'-monophosphate (dAMP), guanosine-5'monophosphate (GMP) and cytidine-5'-monophosphate (CMP) have been examined to assess the photooxidative damage done to these nucleotides under photocatalytic conditions using the cosmetic/sunscreen ZnO pigment. Adsorption of the nucleotide through the phosphate on the positively charged ZnO surface, followed by attack of the ribose/phosphate backbone by photogenerated •OH (and/or •OOH) radicals on the ZnO surface lead to the degradation of the dAMP's ribose moiety and subsequently to decomposition of the adenine base residue. About 90% mineralization of the ribose/phosphate backbone occurred as evidenced by formation of H 2 PO 4 ions after only 30 min of UV irradiation. The nitrogen atoms of the adenine base were converted to NO 3 and NH 4 + ions. About 45% of the organic carbons constituting the dAMP ribose backbone was mineralized to CO 2 within 8 h of UV irradiation occurring through formation of carboxylic acid intermediates (succinic, acetic and formic), with 85% of the remaining nucleobase ultimately mineralized after 48 h of UV irradiation. Similar occurrences were seen for the GMP and CMP

Protective effect of CeO₂ nanoparticles on photo-induced oxidative damage of DNA

“…As an only example, Hidaka et al have reported that photo-deformation of DNA plasmids depends on photocatalytic activity of coexisted oxide semiconductors (ZnO, TiO 2 , CeO 2 ). 25) They confirmed that the undoped and doped CeO 2 had little influence on the DNA damage, but the defensive action of CeO 2 was not mentioned. The present paper demonstrates that the photochemically produced CeO 2 nanoparticles effectively reduce the oxidation rate of DNA due both to the ROS scavenging and UV-light shielding abilities.…”

In vitro genotoxic effects of ZnO nanomaterials in human peripheral lymphocytes

“…In their study, chromatid gaps and chromatid breaks were observed. Hidaka et al (2006) studied the damage of ZnO and various nanoparticles exposed to UV on plasmid DNA via gel electrophoresis method, and demonstrated that ZnO caused faster and larger DNA damage. Dufour et al (2006) studied the effects of ZnO on Chinese hamsters ovary (CHO) cells.…”

DNA Damage Photoinduced by Titanium Dioxide in the Presence of Anionic Vesicles under UV Illumination: Influence of Sodium Chloride Concentration

“…The UV-A radiation (320-400 nm) is the main component of sunlight causing tanning, actinic premature skin aging, dryness and exfoliation and dermatological photosensitivity of the skin and has been implicated in structural and cellular and skin damage [1][2][3][4] . On the other hand, the UV-B radiation (290-320 nm) contributes significantly to erythema and skin cancer 4) .…”

“…Moreover, these pigments are also well-known semiconductor photocatalysts having bandgap energies of 3.2 eV (absorption edge, 387 nm) for TiO 2 anatase and ZnO, and 3.0 eV (414 nm) for TiO 2 rutile. These pigments can generate harmful reactive oxygen species such as O 2 -, HOO and OH radicals when subjected to UV-A/UV-B radiation 2) . Accordingly, these species can cause severe damage of the DNA through strand breaks, as reported in several studies [1][2][3][4][5][6] .…”

“…These pigments can generate harmful reactive oxygen species such as O 2 -, HOO and OH radicals when subjected to UV-A/UV-B radiation 2) . Accordingly, these species can cause severe damage of the DNA through strand breaks, as reported in several studies [1][2][3][4][5][6] . However, some anti-oxidizing agents present in the human body are able to partially protect DNA.…”