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Article Abstract
Acrylamide (AA) is a byproduct of the Maillard reaction, with mitochondrial damage playing a pivotal role in mediating its hepatotoxicity. Allicin, a potent dietary phytochemical, has been used to mitigate the hepatotoxicity of AA. This study confirmed that allicin attenuated mitochondrial structural damage in AA-treated livers and AML-12 cells. Liver RNA-seq analysis identified that Ca transport and nicotinamide adenine dinucleotide (NAD) metabolism, which were associated with mitochondrial function, contributed to the hepatoprotective effects of allicin. Subsequent experiments demonstrated that allicin inhibited AA-caused excessive formation of the mitochondrial-associated endoplasmic reticulum membrane (MAM) and activation of the Ca channel components. Additionally, allicin restored AA-suppressed NAD content and the expression of its dependent deacetylase SIRT3, thereby promoting FoxO3 deacetylation and protecting hepatocytes from mitochondrial Ca overload. Deficiency of SIRT3 eliminated the protective effect of allicin, confirming that allicin antagonized AA-induced hepatotoxicity by regulating mitochondrial Ca homeostasis through the NAD/SIRT3-FoxO3 axis.
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