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The former increases appetite and the latter suppresses appetite, both of which are critical for the metabolic homeostasis of the body (128)
Selective impairment of this carrier-mediated transport can contribute to selective vulnerability of tissues to specific toxins: for example, chronically ethanol-fed hepatocytes become selectively depleted of mitochondrial glutathione because of defective carrier-mediated transport, which makes the hepatocytes susceptible to damage by reactive oxygen species generated from the oxidative metabolism of ethanol (22)
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