Iron chelation reduces intracellular hydroxyl radicals in normal human dermal fibroblasts independently of aging.

Takemoto K, Ozaki A, Tanii Y, Yagi M, Ichihashi M, Ando H.

In cultured skin cells, decreases in antioxidant function and increases in intracellular free Fe2+ due to replicative aging have been reported. The Fenton reaction between Fe2+ and hydrogen peroxide is a threat to the skin because it produces hydroxyl radicals that attack proteins, nucleic acids and lipids. The purpose of this study was to determine whether exogenous iron modulation alters intracellular hydroxyl radicals in senescent normal human dermal fibroblasts (NHDFs). As previously reported, reduced antioxidant function, the accumulation of Fe2+ and increased levels of Reactive Oxygen Species (ROS) were observed in senescent NHDFs. The novel catalase (CAT) activity assay demonstrated a decrease in CAT activity alone in aged NHDFs. However, sufficient CAT activity against hydrogen peroxide was still maintained. Young NHDFs showed an increase in intracellular Fe2+ and hydroxyl radical signals after exogenous iron supplementation, both of which were cancelled by an iron chelator. Under the same experimental conditions, aged NHDFs that already showed a higher concentration of intracellular Fe2+ and stronger hydroxyl radical signals than young NHDFs also elicited a reduction in these levels after the addition of an iron chelator. These results suggest that exogenous regulation of intracellular iron concentration by iron chelators can suppress hydroxyl radical production independently of senescence progression, offering promise for future developments in senescence prevention research.

Antioxidants (Basel)

14

12

1437

10.3390/antiox14121437