This record contains raw data related to the article "N-acetylcysteine Amide AD4/NACA and Thioredoxin Mimetic Peptides Inhibit Platelet Aggregation and Protect against Oxidative Stress"Abstract: In the present study, we tested the effect of small-molecular-weight redox molecules oncollagen-induced platelet aggregation. We used N-acetylcysteine amide (AD4/NACA), the amideform of N-acetylcysteine (NAC), a thiol antioxidant with improved lipophilicity and bioavailabilitycompared to NAC, and the thioredoxin-mimetic (TXM) peptides, TXM-CB3, TXM-CB13, andTXM-CB30. All compounds significantly inhibited platelet aggregation induced by collagen, withTXM-peptides and AD4 being more effective than NAC. The levels of TxB2 and 12-HETE, the mainmetabolites derived from the cyclooxygenase and lipoxygenase pathways following platelet activation,were significantly reduced in the presence of AD4, TXM peptides, or NAC, when tested at thehighest concentration (0.6 mM). The effects of AD4, TXM-peptides, and NAC were also tested onthe clotting time (CT) of whole blood. TXM-CB3 and TXM-CB30 showed the greatest increase in CT.Furthermore, two representative compounds, TXM-CB3 and NAC, showed an increase in the antioxidantfree sulfhydryl groups of plasma detected via Ellman’s method, suggesting a contributionof plasma factors to the antiaggregating effects. Our results suggest that these small-molecularweightredox peptides might become useful for the prevention and/or treatment of oxidative stressconditions associated with platelet activation.

This record contains raw data related to the article "N-acetylcysteine Amide AD4/NACA and Thioredoxin Mimetic Peptides Inhibit Platelet Aggregation and Protect against Oxidative Stress"Abstract: In the present study, we tested the effect of small-molecular-weight redox molecules oncollagen-induced platelet aggregation. We used N-acetylcysteine amide (AD4/NACA), the amideform of N-acetylcysteine (NAC), a thiol antioxidant with improved lipophilicity and bioavailabilitycompared to NAC, and the thioredoxin-mimetic (TXM) peptides, TXM-CB3, TXM-CB13, andTXM-CB30. All compounds significantly inhibited platelet aggregation induced by collagen, withTXM-peptides and AD4 being more effective than NAC. The levels of TxB2 and 12-HETE, the mainmetabolites derived from the cyclooxygenase and lipoxygenase pathways following platelet activation,were significantly reduced in the presence of AD4, TXM peptides, or NAC, when tested at thehighest concentration (0.6 mM). The effects of AD4, TXM-peptides, and NAC were also tested onthe clotting time (CT) of whole blood. TXM-CB3 and TXM-CB30 showed the greatest increase in CT.Furthermore, two representative compounds, TXM-CB3 and NAC, showed an increase in the antioxidantfree sulfhydryl groups of plasma detected via Ellman’s method, suggesting a contributionof plasma factors to the antiaggregating effects. Our results suggest that these small-molecularweightredox peptides might become useful for the prevention and/or treatment of oxidative stressconditions associated with platelet activation.

This record contains raw data related to the article "Albumin Thiolation and Oxidative Stress Status in Patients with Aortic Valve Stenosis".Abstract: Recent evidence indicates that reactive oxygen species play an important causative rolein the onset and progression of valvular diseases. Here, we analyzed the oxidative modifications ofalbumin (HSA) occurring on Cysteine 34 and the antioxidant capacity of the serum in 44 patientswith severe aortic stenosis (36 patients underwent aortic valve replacement and 8 underwent asecond aortic valve substitution due to a degenerated bioprosthetic valve), and in 10 healthy donors(controls). Before surgical intervention, patients showed an increase in the oxidized form of albumin(HSA-Cys), a decrease in the native reduced form (HSA-SH), and a significant reduction in serumfree sulfhydryl groups and in the total serum antioxidant activity. Patients undergoing a second valvereplacement showed levels of HSA-Cys, free sulfhydryl groups, and total antioxidant activity similarto those of controls. In vitro incubation of whole blood with aspirin (ASA) significantly increased thefree sulfhydryl groups, suggesting that the in vivo treatment with ASA may contribute to reducingoxidative stress. We also found that N-acetylcysteine and its amide derivative were able to regenerateHSA-SH. In conclusion, the systemic oxidative stress reflected by high levels of HSA-Cys is increasedin patients with aortic valve stenosis. Thiol–disulfide breaking agents regenerate HSA-SH, thuspaving the way to the use these compounds to mitigate the oxidative stress occurring in the disease

This record contains raw data related to the article "Albumin Thiolation and Oxidative Stress Status in Patients with Aortic Valve Stenosis".Abstract: Recent evidence indicates that reactive oxygen species play an important causative rolein the onset and progression of valvular diseases. Here, we analyzed the oxidative modifications ofalbumin (HSA) occurring on Cysteine 34 and the antioxidant capacity of the serum in 44 patientswith severe aortic stenosis (36 patients underwent aortic valve replacement and 8 underwent asecond aortic valve substitution due to a degenerated bioprosthetic valve), and in 10 healthy donors(controls). Before surgical intervention, patients showed an increase in the oxidized form of albumin(HSA-Cys), a decrease in the native reduced form (HSA-SH), and a significant reduction in serumfree sulfhydryl groups and in the total serum antioxidant activity. Patients undergoing a second valvereplacement showed levels of HSA-Cys, free sulfhydryl groups, and total antioxidant activity similarto those of controls. In vitro incubation of whole blood with aspirin (ASA) significantly increased thefree sulfhydryl groups, suggesting that the in vivo treatment with ASA may contribute to reducingoxidative stress. We also found that N-acetylcysteine and its amide derivative were able to regenerateHSA-SH. In conclusion, the systemic oxidative stress reflected by high levels of HSA-Cys is increasedin patients with aortic valve stenosis. Thiol–disulfide breaking agents regenerate HSA-SH, thuspaving the way to the use these compounds to mitigate the oxidative stress occurring in the disease