China
Africa
Explore chapters and articles related to this topic
Immunomodulatory Activities of Silver Nanoparticles (AgNPs) in Human Neutrophils
Published in Huiliang Cao, Silver Nanoparticles for Antibacterial Devices, 2017
During acute inflammation, PMNs are among the first cells to migrate to an inflammatory site, where they will produce several pro-inflammatory mediators (especially chemokines), attracting other PMNs first and then other cell types, including monocytes, macrophages and lymphocytes; this corresponds to chronic inflammation. The ability of PMNs to eliminate invading pathogens occurs via two important mechanisms. First, the respiratory burst, an oxygen-dependent process, leads to the generation of reactive oxygen species (ROS) known as important messengers and to regulate several functions. Second, degranulation is rather an oxygen-independent mechanism by which PMNs release potent toxic degradative products stored in granules. PMNs are also known as a cellular source of a variety of compounds involved in inflammation, including leukotriene B4, platelet-activating factor and various cytokines such as IL-1α, IL-8, IL-12, TNF-α, TGF-β and GRO-α, to name a few (Edwards and Hallett 1997). Of note, several PMN priming and activating agents such as IL-1β, IL-8, IL-15, GM-CSF, TGF-β, C5a, C9 and so on are found in human fluids in diverse diseases as, for example, in the synovial fluids of rheumatic patients (Cordero et al. 2001; Ottonello et al. 2002; Steiner et al. 1999). These cells are also known to adhere onto cell substratum (e.g. endothelial cells) (Kasper et al. 2006) or onto extracellular matrix proteins, including fibronectin (Anceriz et al. 2007). They can also move toward a chemotactic gradient (chemotaxis) and exert phagocytosis, two important functions also involved in killing and elimination of pathogens. An important new discovery was made concerning the biology of PMNs, one decade ago. Upon activation, PMNs release neutrophil extracellular traps (NETs) composed of decondensed chromatin DNA in association with histones, granular proteins and a few cytoplasmic proteins, which are able to trap and kill extracellular bacteria, fungi and parasites (Brinkmann et al. 2004).
Diazinon toxicity in hepatic and spleen mononuclear cells is associated to early induction of oxidative stress
Published in International Journal of Environmental Health Research, 2022
Manuel Iván Girón-Pérez, Verónica S. Mary, Héctor R. Rubinstein, Gladys A. Toledo-Ibarra, Martín G. Theumer
Besides, oxidative liver damage caused by subchronic or subacute exposure to diazinon in rats was confirmed by measuring the antioxidant levels and lipid peroxidation biomarkers, and the attenuation of increases in aspartate and alanine aminotransferases, alkaline phosphatase, γ-glutamyl transferase and lactate dehydrogenase activities and hepatocellular death by antioxidants (Abdel-Diam et al. 2019; Kalender et al. 2005; Lari et al. 2015; Pourtaji et al. 2016). On the other hand, in vitro studies showed that exposure to high-dose diazinon (250–900 μM) induced ROS and oxidative DNA damage in human cell line of colon carcinoma (HCT116) and hepatoma (HepG2 cells) from 24 h (Boussabbeh et al. 2016) and 48 h (Deferme et al. 2015), respectively. In addition, in the murine monocyte/macrophage cell line RAW264.7, an increase in respiratory burst and a decrease in phagocytic capacity but not a modification in cell viability were observed due to high-level diazinon exposure (150–600 μM) (Ogasawara et al. 2017).
The effect of NADPH oxidase inhibitor diphenyleneiodonium (DPI) and glutathione (GSH) on Isatis cappadocica, under Arsenic (As) toxicity
Published in International Journal of Phytoremediation, 2021
Zahra Souri, Naser Karimi, Parvaiz Ahmad
Arsenic (As) is a toxic metalloid, which broadly distributed in the environment and organisms (Mahimairaja et al. 2005; Ngole-Jeme and Fantke 2017; Hare et al.2018). This toxic element inhibits photosynthesis and disturbs overall metabolic processes (Shahid et al.2019; Sil et al.2019; Souri et al.2020). It has also been demonstrated that, the toxicity of As is associated with the respiratory burst which lead to increase reactive oxygen species (ROS) production, which impairs redox balance and leads to oxidative damage (Souri et al.2017; Souri and Karimi 2017; Souri et al.2018, 2020). Moreover, recent studies suggest that ROS as signaling molecules are involved in numerous developmental processes depending on their content and are regulated via the redox status and antioxidative defense responses (Baxter et al.2014; PÉRez-Chaca et al.2014; Farooq et al.2019; Kushwaha et al.2019).
Lipid peroxidation, serum iron and some antioxidants activities in pregnant women infected with HIV and malaria
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Olufunmilayo A. Idowu, Victoria O. Adekoya, Ayodele S. Babalola, D. Audu, Kehinde O. Ademolu
The blood is an important tissue in man; biochemical parameters are useful in making diagnosis of diseases and also help in the antenatal assessment of women in pregnancy [9]. Hemoglobin degradation by malaria parasite produces the redox active by-products, free heme and H2O2, conferring oxidative stress and damages on the host cell [10]. Apart from hemoglobin degradation, malaria parasitization has been reported to increase oxidative stress through the release of reactive oxygen species (ROS) in patients [11]. In the presence of active malaria parasite infection, phagocytic cells such as polymorphonuclear leukocytes and macrophages usually engage in a respiratory burst as a host cell-mediated immune response. This consequently promotes free radical productions that react to yield ROS. The increase in lipid peroxidation (oxidative stress) level in malaria patients and a decrease in ascorbic acid and GSH (anti-oxidants) have been observed to be accountable for the development of oxidative stress in malaria patients [12]. Hence, malaria parasite virulence seems to depend largely on the patients’ antioxidant capacities, which in turn is determined by the concentrations of antioxidant micronutrients [13].