Oxidative Stress and NO Generation in Cerulein-Induced Acute Pancreatitis in Rats

Тиманн, К.; Шнекенбургер, Ю.; Шик, В.; Demus, Uta; Мюллер-Вердан, У.; Atiakshin, Dmitri; Бекер, В.; Samoilova, Vera; Bukhvalov, I. B.

doi:10.18499/2225-7357-2019-8-1-68-76

Cited by 3 publications

(5 citation statements)

References 35 publications

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“…Application of TSA technology permitted to detect all three NOS isoforms in vascular smooth muscle cells both in the normal pancreas and in pancreatitis [10, 11, 39], like it was earlier shown by us for other tissues [14]. Our findings of NOS expression in vascular smooth muscle cells (Fig.…”

Section: State-of-the-art Immunohistochemical Technology For Nos Detesupporting

confidence: 82%

“…Comparability of protein content in the samples used was confirmed by determination of GAPDH expression (house-keeping protein). These gels are representative of 3 experiments with similar results [39].…”

Section: Figmentioning

confidence: 60%

“…These authors ascribed to NOS3 the role of the main isoform in the pancreas and assumed that NOS3 is protective in the initiation of caerulein-induced acute pancreatitis, though this NOS isoform expression in their experiment did not change during early and inflammatory phases of acute pancreatitis. Contrariwise in our study on the same pancreatitis model, Western blotting of pancreatic NOS protein expression during 48 hr pancreatitis time-course experiments revealed marked NOS1 and NOS3 up-regulation at the time points of 4 and 12 hr [39], which is in agreement with data on NO overproduction by acinar cells found in response to cerulein hyperstimulation at these time points [7]. Remarkably, we detected double bands for NOS3 with a pronounced molecular weight shift to a higher molecular weight at the time points of 4 and 12 hr (Fig.…”

Section: No-generating Enzymes In Pancreasmentioning

confidence: 82%

“…We have shown earlier that oxidative stress runs ahead of NO-synthase (NOS) up-regulation in pancreatic inflammation [10, 11, 39], which implies that the increased NO generation in the course of acute pancreatitis is likely to be an adaptive mechanism aimed at maintaining the homeostatic cellular level of the bioactive NO.…”

Section: No-sgc-cgmp Pathway In Health and Diseasementioning

confidence: 99%

“…This platform allowed us to detect NOS (constitutive isoforms, both NOS1 and NOS3, and an inducible isoform, NOS2) in the human and rat pancreas not only in pancreatic islets, but also in the exocrine compartments and in the vasculature [10, 11, 39]. As an example, we show here the localization of NOS1 and NOS3 with the use of TSA technology in the normal human pancreas in the cytoplasm of acinar cells and in capillaries with a markedly stronger immunostaining of Langerhans islets (Fig.…”

Section: State-of-the-art Immunohistochemical Technology For Nos Detementioning

confidence: 99%

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New Insight into the Role of Nitric Oxide Pathways in Pancreas

Buchwalow

Schnekenburger

Samoilova

et al. 2018

Acta Histochem. Cytochem

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Nitric oxide (NO) is generated by a family of enzymes termed NO synthases (NOS) that convert L-arginine to NO and citrulline. The role of NO as an important biological mediator and recognition of the pathophysiological significance of superoxides/NO interaction has led to an intensive research and development of therapies based on the interception of the NO signaling cascade in the pancreatitis course. However, the presence and localization of the NO-generating enzymes in various organs including pancreas are subject to controversy. We assumed that this controversy might reflect rather the diversity of experimental approaches and an insufficient sensitivity of the methods used. Applying tyramide signal amplification (TSA) immunohistochemical technology, we were able detect all three NOS isoforms both in exocrine and endocrine compartments and in the vasculature in the normal pancreas and in pancreatitis. This also allowed us to demonstrate that oxidative stress runs ahead of NOS up-regulation, which implies that the NO enhancement in the course of pancreatitis is likely to be an adaptive mechanism aimed at maintaining the homeostatic cellular level of the bioactive NO. The aims of this minireview are to describe normal intrapancreatic NO pathways and the role of NO in the pancreatitis course.

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Section: State-of-the-art Immunohistochemical Technology For Nos Detesupporting

confidence: 82%

Section: Figmentioning

confidence: 60%

Section: No-generating Enzymes In Pancreasmentioning

confidence: 82%

Section: No-sgc-cgmp Pathway In Health and Diseasementioning

confidence: 99%

Section: State-of-the-art Immunohistochemical Technology For Nos Detementioning

confidence: 99%

See 3 more Smart Citations

New Insight into the Role of Nitric Oxide Pathways in Pancreas

Buchwalow

Schnekenburger

Samoilova

et al. 2018

Acta Histochem. Cytochem

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Oxygen-Dependent Blood Processes in Beck's Sarcoidosis

Glutkina

Зинчук

2023

Tuberk. bolezni lëgk.

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The objective: to assess the state of oxygen-dependent blood processes in patients with Beck's sarcoidosis.Subjects and Methods. Parameters of blood oxygen transport function and free radical lipid oxidation, as well as the content of nitrogen monoxide and hydrogen sulfide gas transmitters were assessed in the blood of 75 patients (41 women; 34 men) with Beck's sarcoidosis, stage 2 (the pulmonary mediastinal form).Results. In the pulmonary mediastinal form of sarcoidosis versus healthy individuals, there was a decrease in the degree of blood oxygen saturation from 65.4 (60.6; 67.8) to 41.50 (36.0; 49.8), p < 0.05, %, partial oxygen pressure from 40.0 (38.0; 47.0) to 23.0 (18.3; 29.0) mmHg, p < 0.05, and blood pH increased. A decrease in the index of hemoglobin affinity to oxygen p50real (26.80 (24.70; 31.40), p < 0.05, versus healthy individuals 28.2 (27.9; 29.1) mmHg) was revealed. The level of diene conjugates increased in plasma by 86.4% (p < 0.05) and malondialdehyde increased in erythrocytes by 139.2% (p < 0.05), while the following parameters decreased: α-tocopherol (by 42.7 %, p < 0.05), retinol (by 41.9%, p < 0.05), reduced glutathione (by 30.4%, p < 0.05), and ceruloplasmin (by 22.3%, p < 0.05) in plasma. There was an increase in the concentration of nitrogen monoxide (from 15.42 (14.48; 17.71) to 17.09 (7.04; 25.09), mmol/L) and a decrease in hydrogen sulfide (from 29.01 (25.21; 37.03) to 13.08 (8.63; 20.46), mmol/L) in the blood in case of this pathology.Conclusion. There is a deterioration in the blood oxygen-binding properties in patients with Beck's sarcoidosis, stage 2, and as a consequence, tissue needs in oxygen are not adequately provided by blood circulation. There is an increase in the concentration of nitrogen monoxide and a decrease in hydrogen sulfide, which affects the oxygen transport function of blood which may be important for ensuring the processes of oxygen transfer to tissues. In this pathology, activation of lipid peroxidation and a decrease in the level of antioxidant protection factors of blood were revealed which might be important for the genesis of this disease.

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Dishomeostatic phenomena in acute pancreatitis of variable severity

Vlasov,

Al-Kubaisi,

Vlasova

et al. 2024

jour

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Acute pancreatitis remains one of the most dangerous pathologies in the structure of emergency abdominal surgery. This is due to many reasons, including an increase in the frequency of destructive forms of the disease, high mortality, and frequent unfavorable outcomes. The aim of this study was to investigate a number of leading components of homeostasis in patients with acute pancreatitis of varying severity. A retrospective study was conducted on 50 patients with acute pancreatitis of diff erent severity levels who were hospitalized at the Republican Clinical Hospital named after S.V. Katkovа (Saransk, Russia). The patients were divided into groups: the fi rst group (control, n = 30) consisted of patients with mild acute pancreatitis, and the second group (main, n = 20) consisted of patients with severe acute pancreatitis. The study evaluated the endogenous intoxication syndrome, the activity of lipid peroxidation and phospholipase systems, microcirculation status, liver function, and the activity of the coagulation-lytic blood system. The results showed that in the early stages of acute pancreatitis, several pathological processes were observed: the development of endotoxemia syndrome, activation of lipid peroxidation and phospholipase systems, microcirculation disorders, changes in the coagulation and fibrinolytic links of the hemostasis system, and liver function suppression. The severity of these disorders was associated with the severity of the pathology. In cases of mild severity, the changes in the parameters studied were reversible, while in severe cases they were stable and oftenirreversible. The presence of toxemia, oxidative stress, dysmicrocirculation, and hemostatic disorders should be considered as risk factors for disease progression and complications.

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Oxidative Stress and NO Generation in Cerulein-Induced Acute Pancreatitis in Rats

Cited by 3 publications

References 35 publications

New Insight into the Role of Nitric Oxide Pathways in Pancreas

New Insight into the Role of Nitric Oxide Pathways in Pancreas

Oxygen-Dependent Blood Processes in Beck's Sarcoidosis

Dishomeostatic phenomena in acute pancreatitis of variable severity

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