Experimental acute pancreatitis

Xenobiotic Metabolism, Oxidant Stress and Chronic Pancreatitis

“…The first line of evidence has been adduced by measuring the products of lipid peroxidation in a variety of models [4,5], including the new dibutyltin model, which demonstrates the transition from classical acute pancreatitis to chronic pancreatitis within just 60 days [43]. However, the direct demonstration of oxygen free radical activity by dye-coupled fluorescence in the caerulein hyperstimulation model which typically causes oedematous pancreatitis [44], by chemiluminescence in this model and also in the retrograde taurocholate model of haemorrhagic pancreatitis [45], and by electron spin resonance spectroscopy in the CDE model [46] provide unequivocal evidence that oxidant stress is involved at a very early stage in the evolution of experimental acute pancreatitis.…”

“…This paper examines the hypothesis that 'oxidant stress', from altered xenobiotic metabolism rather than from reactive oxygen species alone, depletes glutathione and associated antioxidant defence systems in the pancreatic acinar cell, to set in motion a series of changes leading to chronic pancreatitis [1]. The review begins with a consideration of plant nitrile toxicity because cyanogenic glycosides in dietary staples have been postulated as an aetiological factor in tropical pancreatitis [2,3], and will then dwell upon the complexities of glutathione (GSH) homeostasis and cytochrome P450 (CYP) function, before considering the implications of oxidant stress for acute pancreatitis [4,5], and animal models for each disease.…”

The protective role of melatonin on L-arginine-induced acute pancreatitis in adult male albino rats

“…Oxidative stress plays an important role in acinar cell injury in case of AP, irrespective of the initiating agent or its route of attack [11]. The release of free oxygen radicals may cause direct toxic effects on pancreatic acinar cell leading to its damage [34].…”

Micronutrient ('Antioxidant') Therapy for Chronic Pancreatitis: Basis and Clinical Experience

“…The exocrine pancreas with its huge rate of protein synthesis is particularly vulnerable when subjected to congestion in the busy proteintrafficking lanesan inevitable consequence of pancreastasis episodes, despite the acinar cell's best efforts to compensate by endocrine rerouting of newly synthesised enzymes; removal of zymogen granules via the three-pronged strategy of centripetal dissolution, crinophagy and basolateral redirection; and down-regulation of enzyme synthesis (19,30,34,52). The close integration between oxidative, electrophilic, ER, and inflammation stress is now regarded as the basis for many chronic diseases (177) and, increasingly, for chronic pancreatitis (97,112,123).…”

“…It often presents as an attack that is indistinguishable from acute pancreatitis, representing paralysis of apical exocytosis in acinar cells, 'pancreastasis' (17,19,34), which in animal experiments is tied in with a burst of electron transfer reactions (loosely called free radical activity, FRA) (19,129). Until all secretory parenchyma is obliterated, agonizing pain is usually the predominant symptom, whether accompanying recurrent attacks, or constant and disabling.…”