**5.3 Feverfew PFE reduces DNA damage**

One of the major adverse effects of UV irradiation is damage to DNA. DNA damage by UVB irradiation results from photochemical reactions consequent to direct absorption of photons by DNA bases. The UV-induced DNA lesions that have been studied in most detail are the cyclobutane pyrimidine dimer (CPD) and the 6-4 pyrimidine–pyrimidone photoproduct (6- 4PP) at adjacent pyrimidines (Nakajima et al., 2004). Nuclear DNA strand breaks are produced by incubation of keratinocytes with hydrogen peroxide (Armeni et al., 2001) and hydroxyl radicals, which are generated from hydrogen peroxide through Fe2+-mediated Fenton-type reactions (Stewart et al., 1996).

Fig. 3. Treatment with Feverfew PFE inhibits UV-induced T-T dimer formation.

UV light exposure induces a dose dependent increase in Thymine dimer immunostaining of human skin equivalent tissue. Exposure to 65 kJ/m2 of UV produced a 10-fold increase in T-T dimer formation and 160 kJ/m2 increased T-T dimers approximately 14-fold. Feverfew

of Feverfew PFE. Chromameter, diffused reflectance spectroscopy measurements and independent dermatologist assessment concluded that Feverfew PFE significantly reduced the UV-induced erythema at 24 and 48 hrs after UV exposure (Tierney et al., 2005). This clinical study clearly demonstrates that Feverfew PFE can reduce the skin inflammation and

One of the major adverse effects of UV irradiation is damage to DNA. DNA damage by UVB irradiation results from photochemical reactions consequent to direct absorption of photons by DNA bases. The UV-induced DNA lesions that have been studied in most detail are the cyclobutane pyrimidine dimer (CPD) and the 6-4 pyrimidine–pyrimidone photoproduct (6- 4PP) at adjacent pyrimidines (Nakajima et al., 2004). Nuclear DNA strand breaks are produced by incubation of keratinocytes with hydrogen peroxide (Armeni et al., 2001) and hydroxyl radicals, which are generated from hydrogen peroxide through Fe2+-mediated

**No UV UV UV + Feverfew** 

Fig. 3. Treatment with Feverfew PFE inhibits UV-induced T-T dimer formation.

UV light exposure induces a dose dependent increase in Thymine dimer immunostaining of human skin equivalent tissue. Exposure to 65 kJ/m2 of UV produced a 10-fold increase in T-T dimer formation and 160 kJ/m2 increased T-T dimers approximately 14-fold. Feverfew

damage resulting from UV exposure.

Fig. 2. Feverfew PFE mitigates UV-induced erythema.

**5.3 Feverfew PFE reduces DNA damage** 

Fenton-type reactions (Stewart et al., 1996).

PFE decreased UV induced TT dimer formation by nearly 50% compared to UV alone (Martin etal 2008). Thus the antioxidant properties of Feverfew PFE can block the cascade of events taking place between UV irradiation and DNA damage.

In addition to having direct effects on mitigating DNA damage, Feverfew PFE may also aid the DNA repair process via an indirect mechanism, such as induction of the Nrf2/ARE pathway and downstream activation of several genes involved in oxidative stress response.
