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Similarly, in RBCs from chronic lead-exposed rats, oxidative stress and K + loss were found to accelerate Fas translocation into lipid raft microdomains, inducing Fas-mediated death signaling [169]
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In glutathione metabolism, the endogenous content of glutamate, glycine, 5-oxp, and glutathione (GSH) was significantly increased with the application of 5-oxp under non-stress and heat stress conditions (Fig
We speculated that FA metabolic dysfunction may be the cause of UA-induced cardiomyocyte injury and thereby promote LVR
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