Contribution of RhoA/Rho-kinase/MEK1/ERK1/2/iNOS pathway to ischemia/reperfusion-induced oxidative/nitrosative stress and inflammation leading to distant and target organ injury in rats

Nitric oxide synthase and changes in oxidative stress levels in embryonic kidney observed in a rabbit model of intrauterine growth restriction

“…Prenatal hypoxia has been shown to generate oxidative stress in a variety of animal species . The ROS and reactive nitrogen species produced by NADPH oxidase and iNOS are important mediators of inflammation and organ injury . As expected, we found increased ROS production in the kidneys form restricted fetuses.…”

“…The major sources of reactive oxygen species (ROS) in the vasculature and kidneys are the Nox family of NADPH oxidases, which consists of four Nox proteins (Nox1, Nox2, Nox4, and Nox5) . ROS and NO are important mediators of inflammation and organ injury in kidney . Interestingly, the induction of heme oxygenase‐1 (HO‐1) reduces the production of ROS and may act as a negative modulator of iNOS expression and activity…”

Oxidative damage and nitric oxide synthase induction by surgical uteroplacental circulation restriction in the rabbit fetal heart

“…Our current work aims to further investigate this hypothesis. Nitrogen species produced by iNOS are important mediators of inflammation and oxidative stress damage produced in the heart . We evaluated the oxidative stress damage in the hearts of fetuses under UCR by measuring the protein carbonyl levels.…”

“…Nitrogen species produced by iNOS are important mediators of inflammation and oxidative stress damage produced in the heart. 22 We evaluated the oxidative stress damage in the hearts of fetuses under UCR by measuring the protein carbonyl levels. We found a significant induction of carbonyl levels in the hearts derived from UCR animals ( Figure 4A).…”

Synthesis of N-methylarylnitrones derived from alkyloxybenzaldehydes and antineoplastic effect on human cancer cell lines

“…33 Otherwise, the protein geranylgeranylation can interfere indirectly with the iNOS expression and activity, as demonstrated in the ischemia/ reperfusion injury, which results from activation of RhoA/Rhokinase signaling pathway by RhoA geranylgeranylation and membrane anchorage, leading to increased iNOS expression and activities. 15,34 The geranyl moiety in 1b may interfere with the nitrone property of NO production inhibition by modulating the RhoA/Rhokinase/iNOS signaling pathway. This activity adds pharmacologic value to 1b, and may contribute to its antitumor potential.…”