CuZn-superoxide dismutase, Mn-superoxide dismutase, catalase and glutathione peroxidase in pancreatic islets and other tissues in the mouse

Abstract

Exogenous superoxide dismutase, catalase and scavengers of the hydroxyl radical protect pancreatic-islet cells against the toxic actions of alloxan in vitro [Grankvist et al. (1979) Biochem. J. 182, 17--25]. To test whether the extraordinary sensitivity of islet cells to alloxan is due to a deficiency of endogenous enzymes protecting against oxygen-reduction products, we assayed CuZn-superoxide dismutase, Mn-superoxide dismutase, catalase and glutathione peroxidase in mouse islets and other tissues. To correct for any blood contamination, haemoglobin was also measured in the tissue samples. Pancreatic islets were found to belong to tissues with relatively little activity of the protective enzymes. However, the deviation from other tissues in this respect is probably not large enough to explain the especially great susceptibility of islet cells to alloxan.

Oxidative and nitrosative stress induces peroxiredoxins in pancreatic beta cells

“…Since there are only low concentrations of SOD, CAT and GPX in pancreatic beta cells [6,7,8,9], peroxiredoxins could play an important role as an antioxidant system particularly because, in contrast to these well characterized antioxidant enzymes [8,9,64], gene expression of peroxiredoxins is adjustable by oxidative and nitrosative stress agents. The induction of cellular stress by high glucose, high oxygen, and heat shock treatment has been shown not to affect CAT, SOD or GPX expression in rat pancreatic islets or in RINm5F cells [8].…”

Immunophenotyping of insulitis in control and essential fatty acid deficient mice treated with multiple low-dose streptozotocin

“…In the absence of EFA deficiency, the LDS damage may be amplified by the influx of activated macrophages (single cell insulitis). Islets possess low levels of free radical scavenging enzymes and are, therefore, susceptible to damage by free radicals released by the activated macrophages [25,26]. In addition, these activated macrophages release monokines such as interleukin-1 and tumour necrosis factor which are also cytotoxic to islets [27].…”

Mechanistic Aspects of Alloxan Diabetogenic Activity: A Key Role of Keto−Enol Inversion of Dialuric Acid on Ionization

“…[9][10][11][12][13][14][15][16] The subsequent oxidative decomposition of dialuric acid is thought to account for alloxan toxicity in the -cells through the oxidation stress. [17][18][19] Auto-oxidation of the dialuric acid has been shown to generate O 2 •-, H 2 O 2 , and, in the presence of suitable catalyst, • OH. 5,8,20 It is likely that the potent catalytic effect of transition metals on dialuric acid auto-oxidation is initiated by electron transfer from dialuric acid to metal.…”