Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1692-1700 |
| Number of pages | 9 |
| Journal | Journal Of Investigative Dermatology |
| Volume | 136 |
| Issue number | 8 |
| Early online date | 22 Apr 2016 |
| DOIs | |
| Publication status | Published - 1 Aug 2016 |
Cite this
A powerful mitochondria-targeted iron chelator affords high photoprotection against solar ultraviolet A radiation. / Reelfs, Olivier; Abbate, Vincenzo; Hider, Robert C; Pourzand, Charareh.
In: Journal Of Investigative Dermatology, Vol. 136, No. 8, 01.08.2016, p. 1692-1700.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - A powerful mitochondria-targeted iron chelator affords high photoprotection against solar ultraviolet A radiation
AU - Reelfs, Olivier
AU - Abbate, Vincenzo
AU - Hider, Robert C
AU - Pourzand, Charareh
PY - 2016/8/1
Y1 - 2016/8/1
N2 - Mitochondria are the principal destination for labile iron, making these organelles particularly susceptible to oxidative damage on exposure to ultraviolet A (UVA, 320–400 nm), the oxidizing component of sunlight. The labile iron-mediated oxidative damage caused by UVA to mitochondria leads to necrotic cell death via adenosine triphosphate depletion. Therefore, targeted removal of mitochondrial labile iron via highly specific tools from these organelles may be an effective approach to protect the skin cells against the harmful effects of UVA. In this work, we designed a mitochondria-targeted hexadentate (tricatechol-based) iron chelator linked to mitochondria-homing SS-like peptides. The photoprotective potential of this compound against UVA-induced oxidative damage and cell death was evaluated in cultured primary skin fibroblasts. Our results show that this compound provides unprecedented protection against UVA-induced mitochondrial damage, adenosine triphosphate depletion, and the ensuing necrotic cell death in skin fibroblasts, and this effect is fully related to its potent iron-chelating property in the organelle. This mitochondria-targeted iron chelator has therefore promising potential for skin photoprotection against the deleterious effects of the UVA component of sunlight.
AB - Mitochondria are the principal destination for labile iron, making these organelles particularly susceptible to oxidative damage on exposure to ultraviolet A (UVA, 320–400 nm), the oxidizing component of sunlight. The labile iron-mediated oxidative damage caused by UVA to mitochondria leads to necrotic cell death via adenosine triphosphate depletion. Therefore, targeted removal of mitochondrial labile iron via highly specific tools from these organelles may be an effective approach to protect the skin cells against the harmful effects of UVA. In this work, we designed a mitochondria-targeted hexadentate (tricatechol-based) iron chelator linked to mitochondria-homing SS-like peptides. The photoprotective potential of this compound against UVA-induced oxidative damage and cell death was evaluated in cultured primary skin fibroblasts. Our results show that this compound provides unprecedented protection against UVA-induced mitochondrial damage, adenosine triphosphate depletion, and the ensuing necrotic cell death in skin fibroblasts, and this effect is fully related to its potent iron-chelating property in the organelle. This mitochondria-targeted iron chelator has therefore promising potential for skin photoprotection against the deleterious effects of the UVA component of sunlight.
U2 - 10.1016/j.jid.2016.03.041
DO - 10.1016/j.jid.2016.03.041
M3 - Article
VL - 136
SP - 1692
EP - 1700
JO - Journal Of Investigative Dermatology
JF - Journal Of Investigative Dermatology
SN - 1523-1747
IS - 8
ER -