High dietary carbohydrate and pancreatic lesion

The ability of high dietary carbohydrate to induce acute pancreatitis was investigated in groups of 16, 21-day and 15-month old rats fed different carbohydrate diets for 30 days. Significantly increased levels of serum amylase (2-fold), phospholipids (50 per cent ), phosphorus (2-fold), and lipoperoxides (8-fold) were observed in 15-month old rats fed a high-carbohydrate diet, compared to rats fed a diet with normal carbohydrate levels, indicating peroxidation of membrane lipids which caused final cell death and pancreatic lesion. Serum Cu-Zn superoxide dismutase activity was not altered. Daily administration of bovine Cu-Zn superoxide dismutase conjugated with polyethylene glycol prevented the serum level alterations and pancreatic lesions, indicating that the superoxide radical has a role in dietary carbohydrate-induced acute pancreatitis. No biochemical changes were observed in rats in which treatment was initiated on the 21st day of life indicating that this is an age-related lesion

Nickel chloride effects on erythrocyte generation of superoxide radical

The superoxide anion (O2) is an extremely potent free radical which is produced during the metabolism of aerobic linving cells. (O2) may be involved in lipid peroxidation reactions which occur in a variety of systems. Cu-Zn speroxide dimutase, a metalloprotein, catalyzes the dismutation of the superoxide free radical and protects cells aginst superoxide damage. The ability of NiCl2 to prevent lysis of erythrocytes was tested in rats. NiCl2 administered by intratracheal rouyte prevented hemolysis and decreased total lipids, phospholipids and bilirubin in serum. The protective effect of NiCl2 was linked to an increase in the erytrocyte activity of superoxide dismutase