Acute oxidative stress modulates secretion and repetitive Ca2+ spiking in rat exocrine pancreas

Sweiry, J H; Shibuya, Izumi; Asada, Naoto; Niwa, Koichi; Doolabh, K.; Habara, Yoshiaki; Kanno, Tomio; Mann, Giovanni E.

doi:10.1016/s0925-4439(99)00021-6

Cited by 24 publications

(21 citation statements)

References 38 publications

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“…To determine whether any Ca 2ϩ signaling response or change in cell viability was mediated by free radicals, a further group of cell-agarose constructs was treated with the antioxidant, ascorbate (16,26,29,34). Constructs were incubated in EBSS supplemented with 1 mM ascorbate (Sigma) for 10 min before and throughout the 1-h confocal imaging protocol as indicated in Fig.…”

Section: Methodsmentioning

confidence: 99%

Live cell imaging using confocal microscopy induces intracellular calcium transients and cell death

Knight

Roberts

Lee

et al. 2003

American Journal of Physiology-Cell Physiology

110

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Isolated chondrocytes stained with fluo 4-AM and visualized using standard confocal microscopy techniques exhibited Ca2+ transients and oscillations. Decreasing the power of the laser light decreased the percentage of cells exhibiting these Ca2+ signals. Treatment with the antioxidant ascorbate reduced the Ca2+ response, suggesting that it was mediated by light-induced release of reactive oxygen species (ROS). Cell viability 24 h after the 1-h confocal imaging period was ∼90% for cells that were neither fluorescently stained nor subjected to laser excitation. By contrast, fluorescently stained cells imaged for 1 h exhibited greatly reduced viability. Treatment with ascorbate reduced the level of cell death, suggesting that the effect was mediated by release of exogenous ROS associated with the interaction of light and the fluorochrome. Ca2+oscillations were not always associated with cell death, suggesting that separate light-sensitive pathways mediate the two processes. Light-activated Ca2+ signaling may trigger alterations in numerous cell processes and thereby represent an important and hitherto overlooked artifact in fluorescent microscopy of viable cells.

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Section: Methodsmentioning

confidence: 99%

Live cell imaging using confocal microscopy induces intracellular calcium transients and cell death

Knight

Roberts

Lee

et al. 2003

American Journal of Physiology-Cell Physiology

110

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show abstract

“…In addition to cytosolic calcium impairment, oxidative stress has also been involved in abnormal enzyme acti vation during the early phase of AP [30] . Excessive oxygen radical formation from activated leukocytes [31] leads to oxidative stress and pathological processes. In experimental AP, superoxide radical accumulation could lead to cell cytoskeleton dysfunction leading to intracellular transport impairment and premature activation of digestive enzymes [30] .…”

Section: Initial Pathophysiological Events In Apmentioning

confidence: 99%

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

García

Calvo²

2010

WJGPT

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Acute pancreatitis (AP) is a common and potentially lethal acute inflammatory process. Although the majority of patients have a mild episode of AP, 10%-20% develop a severe acute pancreatitis (SAP) and suffer systemic inflammatory response syndrome (SIRS) and/or pancreatic necrosis. The main aim of this article is to review the set of events, first localized in the pancreas, that lead to pancreatic inflammation and to the spread to other organs contributing to multiorganic shock. The early pathogenic mechanisms in SAP are not completely understood but both premature activation of enzymes inside the pancreas, related to an impaired cytosolic Ca 2+ homeostasis, as well as release of pancreatic enzymes into the bloodstream are considered important events in the onset of pancreatitis disease. Moreover, afferent fibers within the pancreas release neurotransmitters in response to tissue damage. The vasodilator effects of these neurotransmitters and the activation of pro-inflammatory substances play a crucial role in amplifying the inflammatory response, which leads to systemic manifestation of AP. Damage extension to other organs leads to SIRS, which is usually associated with cardiocirculatory physiology impairment and a hypotensive state. Hypotension is a risk factor for death and is associated with a significant hyporesponsiveness to vasoconstrictors. This indicates that stabilization of the patient, once this pathological situation has been established, would be a very difficult task. Therefore, it seems particularly necessary to understand the pathological mechanisms involved in the first phases of AP to avoid damage beyond the pancreas. Moreover, efforts must also be directed to identify those patients who are at risk of developing SAP.

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“…In relation to this, treatment with vitamin C restored impaired Ca 2+ signaling and maintained amylase output impaired by oxidative stress (Sweiry et al, 1999). In a later study, we showed that the oxidant hydrogen peroxide (H 2 O 2 ) inhibited amylase secretion in response to cholecystokinin.…”

Section: Introductionmentioning

confidence: 78%

Melatonin, mitochondria, and Ca2+ homeostasis in the exocrine pancreas: an overview

González¹,

Santofimia-Castaã'o²,

Salido³

2015

Turk J Biol

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Melatonin, a derivative of the amino acid tryptophan, was initially thought to be mainly produced and secreted by the pineal gland; with time, it was also found in other tissues and organs, and even in plants. Since its discovery, the study of the role of the indole in cellular homeostasis has generated impressive data, which have led researchers to a common idea regarding the positive actions of melatonin in health. The uncontrolled production of free radicals in cellular systems leads to the situation termed oxidative stress, which has been signaled as the basis of disease and aging. In the exocrine pancreas, as in other parts of the body, a daily confrontation takes place against oxidative stress. The major signaling mechanisms controlling the physiology of the gland are affected under this situation. Because a love-hate relationship involving mitochondria and oxidative stress has been considered the basis of disease, any physiological regulator that sets hands on the system as a pacemaker will be determinant for the health's fate. Here we present an overview of the recent findings regarding the protective role of melatonin on the function of the exocrine pancreas, paying attention to the role of Ca2+ signaling and the involvement of mitochondria.

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Acute oxidative stress modulates secretion and repetitive Ca2+ spiking in rat exocrine pancreas

Cited by 24 publications

References 38 publications

Live cell imaging using confocal microscopy induces intracellular calcium transients and cell death

Live cell imaging using confocal microscopy induces intracellular calcium transients and cell death

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

Melatonin, mitochondria, and Ca2+ homeostasis in the exocrine pancreas: an overview

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