AI Summary & Key Takeaways
AI InsightAntioxidant enzymes must be consumed in significant amounts to remove the stress produced by ADMA.
📌 3 Key Takeaways
Abstract
Asymmetric dimethylarginine (ADMA) is an inhibitor of nitric oxide synthase (NOS). Oxidative stress might be defined as an imbalance between protein oxidation and antioxidants. Our aim was to determine in vivo whether ADMA causes oxidative damage. Materials and methods: Thirty rats were divided into 3 equal groups: a control group, a group administered 1 mg/kg ADMA, and a group administered 2 mg/kg ADMA. ADMA was administered intraperitoneally for 7 days. Malondialdehyde (MDA), protein carbonyl (PC) content, and nitrate+nitrite concentrations were measured with serum samples. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-Px) activities were analyzed with plasma samples. Results: A significant increase in MDA concentration was observed in the ADMA groups, but this increase was not dose-dependent. However, no significant changes in PC content or nitrate+nitrite concentration were observed. Furthermore, catalase, SOD, and GSH-Px activity was suppressed in the ADMA groups. Suppression of GSH-Px activity was dose-dependent. Conclusion: ADMA results in oxidative damage in vivo with lower doses than in NOS inhibition. ADMA has more of an oxidative effect on lipids than it does on proteins. Antioxidant enzymes must be consumed in significant amounts to remove the stress produced by ADMA.
Özet
Asymmetric dimethylarginine (ADMA) is an inhibitor of nitric oxide synthase (NOS). Oxidative stress might be defined as an imbalance between protein oxidation and antioxidants. Our aim was to determine in vivo whether ADMA causes oxidative damage. Materials and methods: Thirty rats were divided into 3 equal groups: a control group, a group administered 1 mg/kg ADMA, and a group administered 2 mg/kg ADMA. ADMA was administered intraperitoneally for 7 days. Malondialdehyde (MDA), protein carbonyl (PC) content, and nitrate+nitrite concentrations were measured with serum samples. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-Px) activities were analyzed with plasma samples. Results: A significant increase in MDA concentration was observed in the ADMA groups, but this increase was not dose-dependent. However, no significant changes in PC content or nitrate+nitrite concentration were observed. Furthermore, catalase, SOD, and GSH-Px activity was suppressed in the ADMA groups. Suppression of GSH-Px activity was dose-dependent. Conclusion: ADMA results in oxidative damage in vivo with lower doses than in NOS inhibition. ADMA has more of an oxidative effect on lipids than it does on proteins. Antioxidant enzymes must be consumed in significant amounts to remove the stress produced by ADMA.