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These findings suggest that the AMG-mediated decrease in GPx-1-specific activity was caused by loss of a key amino acid at the enzymatic active site

It also may be possible to use detailed phenotyping (QST identified subclinical deficits, thermal hyperalgesia, and individuals more sensitive to chemotherapy) to identify preexisting vulnerabilities for developing OIPN [38,39,40]

Ferroptosis in ocular diseases: mechanisms, crosstalk with other cell death pathways, and therapeutic prospects

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Biswas, P., Dellanoce, C., Vezzoli, A., Mrakic-Sposta, S., Malnati, M., Beretta, A., & Accinni, R
