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Oxidative Stress and Inflammation
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Varsha Rana, Dey Parama, Sosmitha Girisa, Choudhary Harsha, Ajaikumar B. Kunnumakkara
Reactive astrocytes are one of the hallmarks of inflammation and are abundantly found in ALS patients. Increased expression of iNOS is observed in the reactive astrocytes of transgenic mice model of ALS. The upregulation of iNOS produces NO which induces oxidative stress and is correlated with the progressive motor neuronal loss in ALS (Almer et al., 1999; Sasaki et al., 2001). Mitochondrial dysfunction produces increased levels of O2•− which is known to react with NO in the astrocytes to subsequently produce peroxynitrite. The formation of peroxynitrite induces toxicity and oxidative and nitrative stress, which further aggravates mitochondrial dysfunction and eventually causes neuronal death (Cassina et al., 2002; Drechsel et al., 2012, Radi, 2013). Thus, oxidative stress and mitochondrial dysfunction occurring in ALS-astrocytes are vital in the neuronal degeneration during ALS progression as it contributes to excessive ROS production which induces oxidative stress, thereby resulting in a vicious cycle that promotes muscle wasting during the course of ALS (Loeffler et al., 2016).
Nitric Oxide, Sepsis and the Heart
Published in Malcolm J. Lewis, Ajay M. Shah, Endothelial Modulation of Cardiac Function, 2020
Louis H. Alarcon, Timothy R. Billiar, Richard L. Simmons
In addition, nitrosation reactions may occur at other nucleophilic centers under more stringent conditions. For instance, N-nitrosation of DNA and covalent modification of tyrosine residues by peroxynitrite (Beckman et al., 1994), both potential mechanisms of NO toxicity, are more likely to occur in the setting of oxidant stress that deplete the thiol pool (Stamler, 1994). Also, peroxynitrite can result in the production of the highly reactive and toxic hydroxyl radical (OH•) (Beckman et al., 1990). It becomes apparent that while NO and its derived products are potent mediators of microbial and tumor cell killing, they can also inflict significant host tissue damage when NO production is increased.
Burns
Published in Tor Wo Chiu, Stone’s Plastic Surgery Facts, 2018
NO reacts with superoxide free radicals to produce the highly reactive peroxynitrite molecule. It is required for leukocyte-mediated killing and may contribute to resistance to infection and wound healing at later stages of inflammation (Rawlingson A, Burns, 2003). It has been implicated in both the local burn wound inflammation and the systemic inflammatory response to a major burn including pulmonary and cardiovascular dysfunction; dysregulation of NO production is associated with multiple organ failure.
Evaluation of the cardioprotective effect of Casuarina suberosa extract in rats
Published in Drug and Chemical Toxicology, 2022
Ekram Nemr Abd Al Haleem, Samah Fathy Ahmed, Abeer Temraz, Walid Hamdy El-Tantawy
NO is considered a chief molecule contributing to cardiac pathophysiology. Hence, any irregularities in NO synthase and NO metabolism is frequently associated with many heart diseases. Additionally, the stimulation of β- adrenergic receptor by ISO can upregulate/increase inducible NO synthase expression and NO generation in the heart. Consequently, this enhances the production of peroxynitrite through the NO and superoxide radical reaction (Hu et al.2006). Furthermore, enhanced cardiac NO formation by inducible NOx synthase plays a role in myocardial malfunction and death after inducing myocardial infarction in gene knockout mice (Feng et al.2001). It was observed that the selective and continuous prevention of cardiac inducible NO synthase can demonstrate protective effects with regards to myocardial performance, coronary blood flow, cellular infiltration, and decreasing the infarct size (Wildhirt et al.1999). Here, one of the possible cardioprotective mechanisms of the extracts in the ISO-treated rats was their capability to decrease ISO-induced myocardial oxidative stress and membrane impairment (as shown by hindering the exertion of NO and lipid peroxidation in cardiac tissues) by the reactivation of the heart non-enzymatic (GSH) and enzymatic (catalase, GST, SOD). Furthermore, it has been proposed that various flavonoids (Tables 1 and 2) can reduce the generation of NO and subsequent oxidant injury in many pathological circumstances, e.g., infection and inflammation, through the regulation of the inducible nitric oxide synthase (Achike and Kwan 2003).
Anti-inflammatory cytokine IL10 loaded cRGD liposomes for the targeted treatment of atherosclerosis
Published in Journal of Microencapsulation, 2021
Jianchao Li, Fuyan Ding, Xiaoliang Qian, Junjie Sun, Zhenwei Ge, Leiyi Yang, Zhaoyun Cheng
NO is an important reactive metabolite, that is generated inside our body and has major functions as a neurotransmitter and in vasodilation. On contrary to normal physiological conditions, in inflammatory condition generation of NO is elevated. An elevated reactive metabolite NO further reacts with free radicals of ROS family-like superoxide anion (O2•−) to form peroxynitrite (ONOO−) at the atherosclerosis plaque (Kim et al. 2020). Highly reactive oxidant peroxynitrite, causes oxidative damage to the cells, by interacting with proteins and biomolecules such as lipids and nucleic materials likewise DNA. Thereby, to control this damage peroxynitrite generation need to control conversely NO production is a crucial event to pause. Figure 4(B) represented that LPS pre-treatment elevated NO generation by ∼6.5 fold in RAW 264.7 macrophages comparing to control LPS untreated cells. The treatment groups with free IL10, IL10-Lip, and IL10-cRGD-Lip shows reduction in NO production by ∼62% in the LPS pre-treated cells.
Lung macrophages: current understanding of their roles in Ozone-induced lung diseases
Published in Critical Reviews in Toxicology, 2020
Macrophages recognize, engulf, and kill bacteria inside phagolysosomes where NADPH-dependent oxidases produce reactive superoxides, which are further converted to hydrogen peroxide (H2O2) by the enzyme superoxide dismutase (Bedard and Krause 2007). Earlier studies conducted on mice exposed to 0.1 ppm O3 for 3 h revealed that AM from these mice are poor producers of superoxide anions, substrates required for the production of bactericidal H2O2 (Ryer-Powder et al. 1988). Superoxide and nitric oxide (NO) species also react to produce highly reactive peroxynitrite (ONOO−). While superoxides, NO, and ONOO− are essential for creation of the bactericidal microenvironment of lysosomes, they have also been implicated in causing tissue injury (Bedard and Krause 2007).