Time-course of oxygen free radical production in acinar cells during acute pancreatitis induced by pancreatic duct obstruction

Uruñuela, Aránzazu; Sevillano, Sara; Mano, A.M de la; Manso, Manuel A.; Órfão, Alberto; Dios, Isabel De

doi:10.1016/s0925-4439(02)00160-6

Cited by 49 publications

(42 citation statements)

References 27 publications

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“…In AP, there is an excessive production of ROS due to the activation of leukocytes and the formation of proinflammatory interleukins (25). Several studies have reported an increase in MDA levels and a decrease in the activity of antioxidant enzymes (11,(22)(23)(24). In the present study, we observed higher tissue MDA levels and lower CAT and GPx enzyme activity levels in the cerulein group than in the control group.…”

Section: Resultssupporting

confidence: 68%

“…While the mechanism of AP is not fully known, it is believed that reactive oxygen species (ROS) play a major role in the pathogenesis of AP (21,22). Acinar cells have been shown to produce large amounts of ROS in the early stages of AP in rats (23). Reactive oxygen species, such as superoxide anion, H 2 O 2 and the highly reactive hydroxyl radical, are believed to contribute to the etiology of aging and the pathogenesis of a variety of diseases.…”

Section: Resultsmentioning

confidence: 99%

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Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

Batçıoğlu

Gül

Uyumlu

et al. 2009

Braz J Med Biol Res

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The aim of this study was to evaluate the role of oxidative damage in pancreatitis-induced hepatic injury. Thirty-five rats were divided into five groups (each of 7 rats): control, cerulein (100 µg/kg body weight), cerulein and pentoxifylline (12 mg/kg body weight), cerulein plus L-NAME (10 mg/kg body weight) and cerulein plus L-arginine (160 mg/kg body weight). The degree of hepatic cell degeneration differed significantly between groups. Mean malondialdehyde levels were 7.00 ± 2.29, 20.89 ± 10.13, 11.52 ± 4.60, 18.69 ± 8.56, and 8.58 ± 3.68 nmol/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Mean catalase activity was 3.20 ± 0.83, 1.09 ± 0.35, 2.05 ± 0.91, 1.70 ± 0.60, and 2.85 ± 0.47 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively, and mean glutathione peroxidase activity was 0.72 ± 0.25, 0.33 ± 0.09, 0.37 ± 0.04, 0.34 ± 0.07 and 0.42 ± 0.1 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Cerulein-induced liver damage was accompanied by a significant increase in tis sue malondialdehyde levels (P < 0.05) and a significant decrease in catalase (P < 0.05) and GPx activities (P < 0.05). L-arginine and pentoxifylline, but not L-NAME, protected against this damage. Oxidative injury plays an important role not only in the pathogenesis of AP but also in pancre atitis-induced hepatic damage.

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Section: Resultssupporting

confidence: 68%

Section: Resultsmentioning

confidence: 99%

Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

Batçıoğlu

Gül

Uyumlu

et al. 2009

Braz J Med Biol Res

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“…Oxidative stress was documented in pancreatic tissue by detecting generation of ROS with chemiluminescence (Gough et al 1990) or fluorescence (Urunuela et al 2002) and accumulation of products of ROS-mediated lipid peroxidation (Nonaka et al 1989b(Nonaka et al , 1990Guyan et al 1990; Schoenberg et al , 1995Tsai et al 1998;Rau et al 2000) and protein modification (Reinheckel et al 1998), with concomitant depletion of low molecular weight antioxidants (Neuschwander-Tetri et al 1994;Luthen et al 1995;Tsai et al 1998;Schulz et al 1999;Kruse et al 2001;Rau et al 2001;Rahman et al 2004). It was also confirmed by ESR spectroscopy using spin traps (Nonaka et al 1989a).…”

Section: Mechanisms Of Ros and Rns Induced Damage In Pancreatic Acinamentioning

confidence: 97%

Free radicals and the pancreatic acinar cells: role in physiology and pathology

Chvanov

Petersen

Tepikin

2005

Phil. Trans. R. Soc. B

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Reactive oxygen and nitrogen species (ROS and RNS) play an important role in signal transduction and cell injury processes. Nitric oxide synthase (NOS)-the key enzyme producing nitric oxide (NO)-is found in neuronal structures, vascular endothelium and, possibly, in acinar and ductal epithelial cells in the pancreas. NO is known to regulate cell homeostasis, and its effects on the acinar cells are reviewed here. ROS are implicated in the early events within the acinar cells, leading to the development of acute pancreatitis. The available data on ROS/RNS involvement in the apoptotic and necrotic death of pancreatic acinar cells will be discussed.

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“…Oxidative stress has been implicated in the development of acute pancreatitis in diverse animal experimental models, including fatty acid infusion, ischaemia, pancreatic duct obstruction, gallstone pancreatitis and alcohol ingestion, 60,[62][63][64] and measured in patients with mild and severe acute pancreatitis. 65 Previously, we have demonstrated the vital role of Ca 2 þ on MPTP opening in pancreatic acinar cell apoptosis induced by the oxidant menadione.…”

mentioning

confidence: 99%