Melatonin reduces pancreatic tumor cell viability by altering mitochondrial physiology.

Melatonin reduces proliferation in many different cancer cell lines. Thus, melatonin is considered a promising antitumor agent, promoting apoptosis in tumor cells while preserving viability of normal cells. Herein, we examined the effects of melatonin on the pancreatic AR42J tumor cell line.

Melatonin induces calcium release from CCK-8- and thapsigargin-sensitive cytosolic stores in pancreatic AR42J cells.

Melatonin is produced following circadian rhythm with high levels being released at night and has been implicated in the regulation of physiological processes in major tissues, including the pancreas. The aim of our study was to examine the effects of melatonin on intracellular free Ca(2+) concentration ([Ca(2+) ](c)) in AR42J pancreatic cells. Our results show that stimulation of cells with 1 nm cholecystokinin (CCK)-8 led to a transient increase in [Ca(2+) ](c) followed by a decrease towards a value close to the prestimulation level.

Effect of cinnamtannin B-1 on cholecystokinin-8-evoked responses in mouse pancreatic acinar cells.

1. Cinnamtannin B-1 is a naturally occurring A-type proanthocyanidin that belongs to a class of polyphenols widely distributed throughout the plant kingdom and exhibiting anti-oxidant properties. 2.

Increased calcium influx in the presence of ethanol in mouse pancreatic acinar cells.

The effects of alcohol on Ca(2+) signalling remains poorly understood. Here we have investigated the effects of acute ethanol exposure on Ca(2+) influx in mouse pancreatic acinar cells. Cells were loaded with fura-2 and the changes in fluorescence were monitored by spectrofluorimetry and imaging analysis.

Ethanol exerts dual effects on calcium homeostasis in CCK-8-stimulated mouse pancreatic acinar cells.

Background: A significant percentage of patients with pancreatitis often presents a history of excessive alcohol consumption. Nevertheless, the patho-physiological effect of ethanol on pancreatitis remains poorly understood. In the present study, we have investigated the early effects of acute ethanol exposure on CCK-8-evoked Ca2+ signals in mouse pancreatic acinar cells.