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Based on these findings, it was recognized for the first time that impairment of antioxidant defenses (vitamin E-deficiency) and enhanced levels of PUFAs (substrates for LPO) did not just amplify the injury mechanism but switched cell death signaling typically centered around mitochondrial dysfunction (in mice on normal diets) to one dominated by acute LPO [70]

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Food Chem Toxicol 44(1):4255