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found that oxidative stress changed the redox potential of the breast, leading to drastic changes in the DNA base lesions, which are conducive to oxidative conditions and breast cancer formation [64]
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As long as cellular glutathione is above a level considered to be adequate, which is called homeostasis, GCL is inhibited from making gamma-glutamylcysteine (GGC), no matter how much cysteine is available
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In db/db mice and HG-treated TECs, ectonucleoside triphosphate diphosphohydrolase 5 overexpression inhibited apoptosis to preserve TECs via regulating the protein N-glycosylation rate in ER (83)
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