Acute pancreatitis is a disease, which could be manifested as either a mild edematous form or a more severe necrotizing
pancreatitis which has a poor prognosis. The etiology and pathogenesis of this ailment is not completely clear.
Melatonin is an indoleamine which is produced from
L-tryptophan in the pineal gland and in the other tissue including gastrointestinal tract. Both
melatonin and its precursor have been demonstrated to protect the pancreas against
acute pancreatitis and to attenuate pancreatic tissue damage. In the pancreas
melatonin and
L-tryptophan activate complex mechanisms which involve direct scavenging of the
radical oxygen and
nitrogen species, activation of
antioxidant enzymes (
catalase,
superoxide dysmutase, glutation
peroxidase), reduction of pro-inflammatory
cytokines and
prostaglandins, activation of
heat shock protein, and a decrease of
necrosis and increase of regeneration in the pancreas. There are several arguments for the idea that endogenous
melatonin produced in the pineal gland and in the gastrointestinal system could be the part of a native mechanisms for protecting the pancreas against acute damage: 1/ the
melatonin precursor
L-tryptophan exerts similar protective effect as
melatonin, 2/ application of the
melatonin receptor antagonist,
luzindole aggravates
acute pancreatitis, 3/
pinealectomy results in the exacerbation of
acute pancreatitis, 4/ low
melatonin plasma levels are associated with an increased risk of severe
acute pancreatitis. These observations leads to the idea that perhaps
melatonin could be used in clinical trials as supportive
therapy in
acute pancreatitis.