The effect of ionizing radiation on the primate pancreas: An endocrine and morphologic study

Abstract

In this study we evaluated the endocrine, biochemical, and haematological derangements as well as pancreatic and histological changes of the bonemarrow in the primate following external fractionated subtotal marrow irradiation without bonemarrow reconstitution. The irradiation was administered in preparation for pancreatic transplantation. Two groups of animals (ten in each group) received 800 rad (8 Gy) and 1,000 rad (10 Gy) respectively over 4 to 5 weeks. A maximum of 200 rads (2 Gy) were administered weekly as photons from a 6 MV linear accelerator. During irradiation the animals remained normoglycaemic in the presence of transiently elevated liver enzymes and serum amylase values, which returned to normal on completion of the irradiation. Insulin release was significantly reduced in both groups during irradiation and was associated with minimally decreased K-values in the presence of mild glucose intolerance. Pancreatic light morphologic changes included structural changes of both exocrine and endocrine elements and included necrosis of the islet cells and acinar tissue. Islet histology demonstrated striking cytocavitary network changes of alpha and beta cells, including degranulation, vacuolization, mitochondrial destruction, and an increase in lysosomes. A hypoplastic bonemarrow ranging from moderate to severe was observed in all irradiated recipients. Near total fractionated body irradiation in the primate is therefore associated with elevated liver enzymes, pancytopenia, transient hyperamylasaemia, hypoinsulinaemia, a varying degree of pancreatitis, and bonemarrow hypoplasia.

The effect of ultraviolet radiation of pancreatic exocrine cells in mole rats: An ultrastructural study

“…Such degenerative changes that occurred in cytoplasm and organelles resulting in significant functions in each phase of radiation in order that cell could carry on its crucial activities would certainly decrease its process and distort its structure. Our results were in agreement with studies done on some animals tissues due to local irradiation or after high dose radiation (Gridley et al, 2001;Jagetia & Reddy, 2005;Santra & Mannal, 2009), and also some structural studies carried out on living organisms by some researchers (Barcellos-Hoff, 1998;Du Toit et al, 1987;Mansoub & Sarvestani, 2011;Somosy, 2000).…”

“…Some acinar cells were severely damaged and the cytoplasm of cells showed open electron density. These data were corroborated by previous studies done on some animals by investigators (Arulselvan & Subramanian, 2007;Carr et al, 1992;Du Toit et al, 1987;Somosy, 2000).…”

Type 2 Diabetes is a Delayed Late Effect of Whole-Body Irradiation in Nonhuman Primates

“…Short-term studies in baboons have shown morphologic changes to the pancreas and necrosis of pancreatic islet cells and acinar tissue (5). Pancreatic atrophy and exocrine pancreatic insufficiency in response to irradiation have been reported in dog models (26, 27).…”

“…High-dose whole-body irradiation (WBI) (8– 10 Gy cumulatively) injures beta cells and impairs insulin responses to glucose challenge in monkeys in the short term (5), however, less is known about the effects on the important muscle, liver and fat tissues that are involved in glucose disposal (6), production and inflammation, respectively. In the current study, we show the characteristics of a nonhuman primate cohort of monkeys that had been exposed to high-dose radiation 5–9 years earlier and compare these to age-matched nonirradiated monkeys.…”

Abdominal radiation and diabetes: one more piece in the puzzle

“…Indeed, animal studies show that pancreatic radiation results in degranulation, vacuolisation, mitochondrial destruction, and impaired insulin secretion. 5, 6 However, additional functional damage is probably necessary for diabetes to develop. Otherwise, we would expect diabetes to occur in childhood, rather than young adulthood, that the risk would not plateau at 20–29 Gy, and that there would be a preponderance of type 1 diabetes.…”