UV-induced DNA damage in skin cells is an important initiator of signaling pathways. The DNA photoproducts generated by UV-induced DNA damage are altered DNA structures that activate a cascade of responses, beginning with the initiation of cell cycle arrest and activation of DNA repair mechanisms. The biologically harmful effects associated with UV radiation exposure are largely the result of errors in DNA repair, which can lead to oncogenic mutations [reviewed in 86]. UV-induced DNA damage in the form of cyclobutane pyrimidine dimers (CPD) is considered as a molecular trigger for the induction of immunosuppression and initiation of photocarcinogenesis [52, 100]. Several studies have documented that exposure of the skin to UV radiation results in immediate formation of CPDs in skin cells . Most of the UVB-induced CPDs were found in the epidermis, but some were detected in the dermis. The location of the damage depends on the ability of the UV radiation to penetrate the skin . It has been found that UV exposure of less than one minimal erythema dose is sufficient to cause damage DNA in target cells of human skin .
UVB-induced CPDs are formed immediately after the interaction of photons with the DNA molecule. In an in vitro study using cultured human cells (lung fibroblasts, skin fibroblasts, and epidermal keratinocytes), EGCG resulted in a dose-dependent reduction in UV-induced DNA damage in all three cell types . When applied topically to the mouse skin, GTPs (a mixture of green tea polyphenols) significantly inhibited UVB-induced DNA damage as assessed using a 32P-postlabelling technique . Topical treatment of human skin with GTPs prior to UV exposure resulted in a dose-dependent inhibition of formation of CPDs . Camouse et al.  found that topical application of green tea or white tea extracts provided human skin protection from solar-simulated ultraviolet light. These tea extracts were shown to provide protection against the detrimental effects of UV light on cutaneous immunity. The investigators concluded that these protective effects were not due to direct UV absorption or sunscreen effects as both products had a sun protection factor of 1.
Extensive studies of the effects of polyphenols, particularly green tea polyphenols, on the repair kinetics and repair mechanisms of UV-induced CPDs have been carried out in the laboratory of Dr. Katiyar. One of these studies showed that topical treatment of skin with EGCG does not prevent UVB-induced formation of CPDs immediately after UVB irradiation, which indicated that EGCG does not have a significant filtering effect on the UVB radiation. However; in skin samples obtained at 24 hours or 48 hours after UVB exposure, the numbers of CPD-positive cells were significantly reduced (or repaired) in the EGCG-treated C3H/HeN mouse skin as compared to the control group of mice which were not treated with EGCG . Studies of the DNA repair mechanisms suggested that the rapid repair of UV-induced CPDs by EGCG was mediated through stimulation of a cytokine (IL-12) on application of the EGCG onto the mouse skin . IL-12 has been shown to have the capacity to induce DNA repair [62, 79, 80] and this concept was confirmed by testing the effect of EGCG on UV-induced CPD formation in IL-12 knockout mice. EGCG does not remove or repair UV-induced CPDs in the skin of IL-12 knockout mice, further confirming the role of IL-12 in rapid repair of DNA damage by this polyphenol . Studies of the effects of oral administration of GTPs in the drinking water of mice on UVB-induced DNA damage also were carried out and it was found that UV-induced DNA damage (CPDs) was resolved rapidly in the GTPs-treated mice when compared to GTPsuntreated mice . This DNA repairing effect of GTPs was less pronounced in IL-12 knockout mice, as was observed in the case of EGCG treatment. Schwarz et al.  observed that treatment of normal human keratinocytes and “human skin equivalent” with GTPs reduced UVB-induced DNA damage and that this effect was mediated through the induction of IL-12. Collectively, these data suggest that the difference in the GTPs-associated DNA repair capacity between IL-12 knockout mice and their wild-type counterparts may be due to the absence of IL-12 in the IL-12 knockout mice. The mechanisms by which GTPs repaired CPDs were identical to the mechanisms by which EGCG repaired CPDs.
Wei et al.  have shown that an aqueous extract of green tea scavenges H2O2 and inhibits UV-induced oxidative DNA damage in an in vitro system. Zhao et al.  demonstrated that application of green tea extract to Epiderm, a reconstituted human skin equivalent, also inhibited psoralen-UVA-induced formation of 8-methoxypsoralen-DNA adducts . Treatment of skin with a 5% green tea extract significantly inhibited DNA damage induced by solar simulator radiation when assessed using a 32P-postlabeling technique . These observations demonstrate the potential chemopreventive effects of green tea polyphenols against UVB-induced DNA damage.
Repair of UV-induced DNA damage by green tea polyphenols is mediated through nucleotide excision repair (NER) mechanism
Further studies have been conducted to verify the green tea polyphenol-associated DNA repair mechanisms in UVB-irradiated skin. Meeran et al. postulated that an NER mechanism is involved in the repair of photodamaged DNA by green tea polyphenols, and that IL-12 has a role in this process [61, 63]. To determine whether the NER mechanism is required for the EGCG-induced IL-12-mediated repair of UVB-induced CPDs, NER-deficient fibroblasts from xeroderma pigmentosum complementation group A (XPA) patients and NER-proficient fibroblasts from a healthy person (XPA-proficient) were exposed to UVB with or without prior treatment with EGCG. The CPD-positive cells were detected by immunostaining at different time points after UVB exposure of the cells. It was observed that the numbers of CPD-positive cells were significantly lower at 24 hours after UVB exposure in the XPA-proficient cells, but that treatment with EGCG did not significantly remove or repair UVB-induced CPDs in NER-deficient cells. This observation indicated that EGCG-induced DNA repair is mediated through a functional NER mechanism.