Читать книгу Drug Transporters - Группа авторов - Страница 58

An Octn1 ^−/− knockout mouse was developed with a complete deletion of exon 1 [84]. Octn1 ^−/− mice are fertile, viable, and have no gross physiological abnormalities. These mice exhibit systemic depletion of ergothioneine compared to wild‐type, which has high tissue accumulation of ergothioneine in the small intestine and kidney. Octn1 ^−/− mice subjected to intestinal oxidative stress have significantly lower tolerance for the oxidative stress and worse survival outcomes compared with wild‐type mice, suggesting that ergothioneine’s antioxidant properties contribute to protection or recovery from oxidative stress. Additionally, knockout of Octn1 results in increased kidney damage measured by oxidative stress and interstitial fibrosis in a mouse model of chronic kidney disease (CKD) [85].