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The main pathway for elimination of acrolein is conjugation with glutathione (GSH) in the liver, followed by enzymatic cleavage of the γ-glutamic acid and glycine residues, respectively, in the liver and in the kidney [58, 59], and N -acetylation of the resultant cysteine conjugate to form S -(3-oxopropyl)- N -acetylcysteine (OPMA) in the kidney
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its impairment leads to dysfunctional mitochondria accumulation, increasing oxidative damage and ferroptosis (64)
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