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- W3172569550 abstract "Aldehyde dehydrogenase 2 (ALDH2) is important for the detoxification of 4-hydroxy-2-nonenal (HNE), a toxic aldehyde produced by oxidative stress-induced lipid peroxidation, which can form protein adducts and alter cell function. Tolerance to nitrates such as nitroglycerin (GTN) is associated with oxidative stress, inactivation of ALDH2, and decreased GTN-induced cGMP accumulation and vasodilation. We hypothesized that GTN-induced inactivation of ALDH2 results in increased HNE adduct formation of key proteins, and consequently an altered vasodilator response to GTN. This was assessed in a cell culture model (PK1 cells), and in aortae from GTN-tolerant rats and ALDH2 null mice. Immunoblot analysis indicated a marked increase in HNE adduct formation in all three preparations. Preincubation of PK1 cells with HNE resulted in a dose-dependent decrease in GTN-induced cGMP accumulation, and pretreatment of isolated rat aorta with HNE resulted in dose-dependent decreases in the vasodilator response to GTN, thus mimicking GTN-tolerance. Pretreatment of aortae from ALDH2 null mice with 10 μM HNE also resulted in a desensitized vasodilator response, and mimicked the desensitized response observed in GTN tolerance. The data are consistent with the notion of a primary role of HNE protein adduct formation in the development of GTN tolerance. This work was supported by grant from the Canadian Institutes of Health Research (MOP 81175)" @default.
- W3172569550 created "2021-06-22" @default.
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- W3172569550 date "2013-04-01" @default.
- W3172569550 modified "2023-09-25" @default.
- W3172569550 title "Role of the lipid peroxidation product, 4‐hydroxynonenal, in the in the development of nitrate tolerance" @default.
- W3172569550 doi "https://doi.org/10.1096/fasebj.27.1_supplement.676.3" @default.
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