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Zhang YL et al. · Redox biology ·
C57BL/6 mice were exposed to a single high dose of radiation aimed at the chest, which injures the lungs, and then half were given daily injections of R13A-MOTS-c at 5 mg per kilogram of body weight for two weeks while the others got no treatment. The peptide is a modified version of a natural protein fragment, with one amino acid swapped to make it less polar so it can cross cell membranes more easily. In the lab, the researchers also grew mouse lung cells in dishes and exposed them to radiation, then added the peptide to some of them. They measured markers of inflammation, oxidative stress, and damage to mitochondria, the energy-producing parts of cells, in both the mice and the cultured cells. The paper reports that the treated mice and cells showed lower levels of these damage markers, and that this effect depended on the peptide entering cells through a specific transporter called LAT1 and activating a protective signaling pathway called Nrf2. When the researchers blocked LAT1 or Nrf2, the protective effects disappeared.
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