New Kind of Sunscreen Targeting Free Iron in Cells May Also Treat Friedrich’s Ataxia
A new form of sun protection that works by chelating, or binding, excess iron within mitochondria may not only protect against UVA rays that current lotions are unable to block, but also lead to new treatments for Friedreich’s ataxia (FA). The compound, named “mitoiron claw” by the scientific team in the U.K. that developed it, is thought capable of reducing excess mitochondrial iron, a cause of FA.
Most sunscreens protect against UVB radiation in sunlight but are largely ineffective against UVA rays, which are most damaging to iron concentrations in cells. The mitoiron claw compound works by chelating iron (or binding to an iron atom like a claw) to remove excessive iron from in the body. The researchers — from the University of Bath and King’s College London — are hoping to have it commercially available in sunscreen and skin care products in about four years.
Mitochondria, the energy powerhouses of cells, are particularly high in free iron concentrations used for a number of cellular functions. But when exposed to UVA radiation, this free iron acts as a catalyst in the production of toxic reactive oxygen species (ROS), which damages a cell’s DNA, proteins and fat, and can cause cell death. The new compound targets mitochondria to bind the excess free iron there and prevent it from reacting to UVA rays.
In the study, “A Powerful Mitochondria-Targeted Iron Chelator Affords High Photoprotection against Solar Ultraviolet A Radiation, published in the Journal of Investigative Dermatology ,the researchers exposed skin cells to UVA radiation equivalent to 140 minutes of uninterrupted sun exposure. Those skin fibroblast cells treated with the mitoiron claw were seen to be protected against cell death, while untreated cells died in significant numbers.
“The role of iron-mediated damage induced upon exposure of skin cells to UVA has been underestimated for many years. For efficient protection against UVA-induced iron damage of skin strong chelators are needed, but until now these risked toxic effects caused by non-targeted iron starvation of cells,” Dr. Charareh Pourzand, with the Department of Pharmacy and Pharmacology at Bath, said in a news release. “Our mitochondria-targeted compound provides a solution to this problem.”
The researchers plan to also look into other applications for the compound, including its utility in treating diseases like Friedreich’s ataxia that are linked to iron overload in mitochondria.