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Obermannov, R
These alterations can modulate immune mechanisms, including T-cell polarization and autoantibody generation, thereby playing a role in the pathogenesis of HT (Lee et al
Artificial overexpression of GPx1 showed an increased capacity to rescue breast cancer cells from the cell cycle arrest caused by hyperoxic stress, indicating the involvement of both peroxide-derived free radicals and nonperoxide-derived species during the deleterious process [84]
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