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To determine whether the colistin-induced depolarization was the result of the opening of the mitochondrial permeability transition pore (mPTP), mitochondria were co-incubated with colistin and cyclosporin A, a well-characterized desensitizer of the mPTP 31,32

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Interestingly, one recent study found that intestinal sirtuin 1 (SIRT1) deficiency could normalize ethanol-induced increase of hepatic iron to nearly control levels, suggesting that SIRT1 plays a crucial role in the iron overload in ALD [87]