scholarly journals Regulation of Superoxide by BAP31 through Its Effect on p22phox and Keap1/Nrf2/HO-1 Signaling Pathway in Microglia

2021 ◽  
Vol 2021 ◽  
pp. 1-27
Author(s):  
Xia Liu ◽  
Qing Yuan ◽  
Guo-xun Li ◽  
Cong-cong Jia ◽  
Jing-yu Liu ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Superoxide Anion ◽  
Neuronal Damage ◽  
Oxidase Inhibitor ◽  
Superoxide Anion Production ◽  
Regulatory Molecule ◽  
Bv2 Cells ◽  
Anion Production

Reactive oxygen species (ROS) production by activation of microglia is considered to be a major cause of neuronal dysfunction, which can lead to damage and death through direct oxidative damage to neuronal macromolecules or derangement of neuronal redox signaling circuits. BAP31, an integral ER membrane protein, has been defined as a regulatory molecule in the CNS. Our latest studies have found that BAP31 deficiency leads to activation of microglia. In this study, we discovered that BAP31 deficiency upregulated LPS-induced superoxide anion production in BV2 cells and mice by upregulating the expression level of p22phox and by inhibiting the activation of Nrf2-HO-1 signaling. Knockdown of p22phox/keap1 or use of an NADPH oxidase inhibitor (apocynin) reversed the production of superoxide anion and inflammatory cytokines, which then reduced neuronal damage and death in vitro and in vivo. These results suggest that BAP31 deficiency contributes to microglia-related superoxide anion production and neuroinflammation through p22phox and keap1. Furthermore, the excess superoxide anion cooperated with inflammatory cytokines to induce the damage and death of neurons. Thus, we determined that BAP31 is an important regulator in superoxide anion production and neuroinflammation, and the downstream regulators or agonists of BAP31 could therefore be considered as potential therapeutic targets in microglial-related superoxide anion production and neuroinflammation.

Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells

1992 ◽  
Vol 262 (1) ◽  
pp. L63-L68 ◽  
Author(s):  
R. S. Oosting ◽  
J. F. Van Iwaarden ◽  
L. Van Bree ◽  
J. Verhoef ◽  
L. M. Van Golde ◽  
...  
Keyword(s):  
Superoxide Anion ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Alveolar Type ◽  
Type Ii ◽  
Superoxide Anion Production ◽  
Anion Production

This study focused on the question of whether exposure of surfactant protein A (SP-A) to ozone affected properties of this protein that may be involved in regulating alveolar type II cell and alveolar macrophage functions. In vitro exposure of human or canine SP-A to ozone reduced the ability of this protein to inhibit phorbol-ester induced secretion of [3H]phosphatidylcholine by alveolar type II cells in culture. Ozone-exposed human SP-A showed a decreased ability to enhance phagocytosis of herpes simplex virus and to stimulate superoxide anion production by alveolar macrophages. Experiments with elastase showed that ozone-exposed canine SP-A was more susceptible to proteolysis. A conformational change of the protein could underlie this phenomenon. Surfactant isolated from ozone-exposed rats (0.4 ppm ozone for 12 h) was also less able to stimulate superoxide anion production by alveolar macrophages than surfactant from control rats, which suggested that SP-A in vivo was also susceptible to ozone. The results of this study suggest that SP-A-alveolar cell interactions can be inhibited by ozone exposure, which may contribute to the toxicity of ozone in the lungs.

Polysaccharides from the green alga Caulerpa racemosa (Agardh, 1873) improve the immune response and antioxidant status in the white shrimp Litopenaeus vannamei (Boone, 1931) (Dendrobranchiata, Penaeidae)

Crustaceana ◽  
2020 ◽  
Vol 93 (6) ◽  
pp. 611-632
Author(s):  
Po-Tsang Lee ◽  
Meng-Chou Lee ◽  
Yi-Tien Ho ◽  
Zhen-Hao Liao ◽  
Huai-Ting Huang ◽  
...  
Keyword(s):  
Litopenaeus Vannamei ◽  
Superoxide Anion ◽  
Production Capacity ◽  
White Shrimp ◽  
Feed Additive ◽  
Caulerpa Racemosa ◽  
Superoxide Anion Production ◽  
Anion Production

Abstract The objective of this study was to investigate the effects of Caulerpa racemosa (Agardh, 1873) polysaccharides (CRP) on non-specific immunity of the white shrimp, Litopenaeus vannamei (Boone, 1931). The extracted polysaccharide consists of galactose, glucose, and mannose. Total polyphenolic compound and total flavonoids content in CRP were determined. In vitro CRP treatment did not alter cell viability of haemocytes and significantly activated phenoloxidase (PO) activity, superoxide anion production capacity, phagocytic rate, and index in haemocytes. Immune parameters, such as total haemocyte count, PO activity, phagocytosis, and superoxide anion production, were significantly elevated in CRP-fed shrimp during the rearing period. Malondialdehyde levels in the hepatopancreas of CRP-fed shrimp were lower than in control shrimp from day 7 to day 28. These results show that CRP exhibits antioxidant activity and can activate immune responses of white shrimp in vitro and in vivo. Therefore, CRP can be considered a functional feed additive to improve white shrimp immunity.

Mechanisms towards compensation of long-term haemopoietic injury in mice after 5 Gy irradiation: In vivo and in vitro enhancement of superoxide anion production by granulocytes

1992 ◽  
Vol 12 (4) ◽  
pp. 281-292 ◽  
Author(s):  
Soledad Gaitán ◽  
Elvira Cuenllas ◽  
Pilar Sancho ◽  
Juan A. Bueren ◽  
Concepción Tejero
Keyword(s):  
Superoxide Anion ◽  
Environmental Damage ◽  
X Rays ◽  
Superoxide Anion Production ◽  
Protein Levels ◽  
Anion Production ◽  
Bone Marrow Cultures

This paper analyzes the long-term (6 and 12 months) function of mouse granulocytes after total body irradiation with a single dose (5 Gy) of X-rays. Superoxide anion production has been investigated in granulocytes from peripheral blood, and also in those harvested from long term bone marrow cultures, with the aim of correlating the environmental damage induced by radiation with the functional properties of granulocytes. An in vivo and in vitro enhancement of superoxide anion production and protein levels in granulocytes from irradiated mice is described. The presence of some colony stimulating factor in the supernatant of cultures from irradiated mice could play an important role in the priming of granulocytes.

Mitochondrial Adenosine Triphosphate–regulated Potassium Channel Opening Acts as a Trigger for Isoflurane-induced Preconditioning by Generating Reactive Oxygen Species

2003 ◽  
Vol 98 (4) ◽  
pp. 935-943 ◽  
Author(s):  
Katsuya Tanaka ◽  
Dorothee Weihrauch ◽  
Lynda M. Ludwig ◽  
Judy R. Kersten ◽  
Paul S. Pagel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Infarct Size ◽  
Adenosine Triphosphate ◽  
Superoxide Anion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Superoxide Anion Production ◽  
Channel Opening ◽  
Anion Production

Background Whether the opening of mitochondrial adenosine triphosphate-regulated potassium (K(ATP)) channels is a trigger or an end effector of anesthetic-induced preconditioning is unknown. We tested the hypothesis that the opening of mitochondrial K(ATP) channels triggers isoflurane-induced preconditioning by generating reactive oxygen species (ROS) in vivo. Methods Pentobarbital-anesthetized rabbits were subjected to a 30-min coronary artery occlusion followed by 3 h reperfusion. Rabbits were randomly assigned to receive a vehicle (0.9% saline) or the selective mitochondrial K(ATP) channel blocker 5-hydroxydecanoate (5-HD) alone 10 min before or immediately after a 30-min exposure to 1.0 minimum alveolar concentration (MAC) isoflurane. In another series of experiments, the fluorescent probe dihydroethidium was used to assess superoxide anion production during administration of 5-HD or the ROS scavengers N-acetylcysteine or N-2-mercaptopropionyl glycine (2-MPG) in the presence or absence of 1.0 MAC isoflurane. Myocardial infarct size and superoxide anion production were measured using triphenyltetrazolium staining and confocal fluorescence microscopy, respectively. Results Isoflurane (P < 0.05) decreased infarct size to 19 +/- 3% (mean +/- SEM) of the left ventricular area at risk as compared to the control (38 +/- 4%). 5-HD administered before but not after isoflurane abolished this beneficial effect (37 +/- 4% as compared to 24 +/- 3%). 5-HD alone had no effect on infarct size (42 +/- 3%). Isoflurane increased fluorescence intensity. Pretreatment with N-acetylcysteine, 2-MPG, or 5-HD before isoflurane abolished increases in fluorescence, but administration of 5-HD after isoflurane only partially attenuated increases in fluorescence produced by the volatile anesthetic agent. Conclusions The results indicate that mitochondrial K(ATP) channel opening acts as a trigger for isoflurane-induced preconditioning by generating ROS in vivo.

Acute infusion of nicotine impairs nNOS-dependent reactivity of cerebral arterioles via an increase in oxidative stress

2007 ◽  
Vol 103 (6) ◽  
pp. 2062-2067 ◽  
Author(s):  
Denise M. Arrick ◽  
William G. Mayhan
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Potential Role ◽  
Acute Exposure ◽  
Cerebral Microcirculation ◽  
Superoxide Anion Production ◽  
Anion Production ◽  
Cerebral Arterioles ◽  
Oxide Synthase

Our goals were to determine whether acute exposure to nicotine alters neuronal nitric oxide synthase (nNOS)-dependent reactivity of cerebral arterioles and to identify a potential role for oxidative stress in nicotine-induced impairment in nNOS-dependent responses of cerebral arterioles. We measured in vivo diameter of cerebral arterioles to nNOS-dependent ( N-methyl-d-aspartate and kainate) and -independent (nitroglycerin) agonists before and during acute treatment with nicotine. We found that nNOS-dependent, but not -independent, vasodilatation was impaired during treatment with nicotine. In addition, treatment of the cerebral microcirculation with tempol (1 h before infusion of nicotine) prevented nicotine-induced impairment in nNOS-dependent vasodilatation. Furthermore, the production of superoxide anion (lucigenin chemiluminescence) was increased in parietal cortex tissue of rats by treatment with nicotine, and this increase in superoxide anion production could be inhibited by tempol. Our findings suggest that acute exposure to nicotine impairs nNOS-dependent dilatation of cerebral arterioles by a mechanism that appears to be related to the formation of superoxide anion.

scholarly journals Mitochondria Superoxide Anion Production Contributes to Geranylgeraniol-Induced Death inLeishmania amazonensis

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Milene Valéria Lopes ◽  
Vânia Cristina Desoti ◽  
Angelo de Oliveira Caleare ◽  
Tânia Ueda-Nakamura ◽  
Sueli Oliveira Silva ◽  
...  
Keyword(s):  
Superoxide Anion ◽  
Chromatin Condensation ◽  
Ultrastructural Changes ◽  
Resonance Imaging ◽  
Superoxide Anion Production ◽  
Human Blood Cells ◽  
Anion Production ◽  
Bioactive Constituent ◽  
Intracellular Amastigote

Here we demonstrate the activity of geranylgeraniol, the major bioactive constituent from seeds ofBixa orellana, againstLeishmania amazonensis. Geranylgeraniol was identified through1H and13C nuclear magnetic resonance imaging and DEPT. The compound inhibited the promastigote and intracellular amastigote forms, with IC50of11±1.0and17.5±0.7 μg/mL, respectively. This compound was also more toxic to parasites than to macrophages and did not cause lysis in human blood cells. Morphological and ultrastructural changes induced by geranylgeraniol were observed in the protozoan by electronic microscopy and included mainly mitochondria alterations and an abnormal chromatin condensation in the nucleus. These alterations were confirmed by Rh 123 and TUNEL assays. Additionally, geranylgeraniol induces an increase in superoxide anion production. Collectively, ourin vitrostudies indicate geranylgeraniol as a selective antileishmanial that appears to be mediated by apoptosis-like cell death.

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