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Here, working primarily in mouse hepatocytes, we show that decreasing the availability of substrate for the TCA cycle diminished NADPH production and attenuated ER stress in a manner that depended on glutathione oxidation

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Through diverse delivery mechanisms, the more effective and safer radioprotective strategies become achievable

Exposure to PTU resulted in severe thyroid hormone depletion in both serum and brain, accompanied by structural brain abnormalities, whereas PCN primarily induced hepatic enzyme activity with minimal effect on circulating thyroid hormone levels

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