Pancreatic acinar cell necrosis with intact storage of digestive enzymes in selenomethionine treated rats.
Morphological and biochemical changes were observed in the pancreas and serum of rats after the intraperitoneal administration of selenomethionine, sodium selenite and methionine. Selenomethionine caused rapidly developing acinar cell necrosis. The first pathological changes were mitochondrial swelling and flocculent densities, and dilatation of cisternae of the endoplasmic reticulum. Zymogen granules appeared disrupted only in disintegrated acinar cells. Signs of autodigestive pancreatic inflammation with fat necrosis, elevation of pancreatic phospholipase A2 and serum amylase activities, as well as pulmonary oedema were present. Sodium selenite caused similar histologic changes to those produced by selenomethionine, but no changes were seen after methionine administration. Destruction of pancreatic acinar cells by an intraductal oleic acid injection that resulted in exocrine atrophy did not prevent systemic selenomethionine toxicity. Our results show that selenomethionine causes pancreatic acinar cell necrosis and that intracellular transport and storage of digestive enzymes is not primarily altered by this chemical.
Hietaranta
A J
AJ
Department of Pathology, University of Turku, Finland.
Nevalainen
T J
TJ
Aho
H J
HJ
Hämäläinen
O M
OM
Suortamo
S H
SH
D000818:Animals; D008297:Male; D008854:Microscopy, Electron; D009336:Necrosis / Q000139:chemically induced; D010179:Pancreas / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium / Q000633:toxicity*; D012645:Selenomethionine / Q000633:toxicity*; D018038:Sodium Selenite
D012645:Selenomethionine; D012643:Selenium; D018038:Sodium Selenite