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Catalase expression in pancreatic alpha cells of diabetic and non-diabetic mice

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Abstract

The pancreatic islet beta cells are very sensitive to oxidative stress, probably due to the extremely low level of anti-oxidant enzymes, particularly catalase. In contrast to beta cells, pancreatic alpha cells are significantly more resistant to diabetogenic toxins. However, whether alpha cells express a different level of catalase is not known. The aim of this study was to evaluate catalase expression in alpha cells of diabetic and non-diabetic mice. Diabetes was induced by a single injection of streptozotocin. After 3 weeks of persistent hyperglycemia, pancreatic tissues were collected. Catalase localization in alpha cells was identified by a dual-immunofluorescence staining with anti-glucagon and anti-catalase antibodies. In intact mice, intensive catalase and glucagon immunostaining was found in the peripheral area of islets. Merged images of glucagon and catalase show their localization in the same cell type, namely, alpha cells. Confocal microscopy indicated that the glucagon and catalase staining was distributed throughout the cytoplasm. Similar co-expression of catalase and glucagon was found in the alpha cells of diabetic animals. The results of this study show the intensive catalase expression in alpha cells of diabetic and non-diabetic mice. This knowledge may be useful to better understand the defense mechanisms of pancreatic alpha cells against oxidative stress.

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Acknowledgments

This study was supported by a grant from the Research Foundation of Sackler Faculty of Medicine, Tel Aviv University. We thank Pepy Roizman for excellent assistance in the immunohistochemical study, and Sara Dominitz for editing the manuscript.

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Correspondence to Konstantin Bloch.

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Bloch, K., Shichman, E., Vorobeychik, M. et al. Catalase expression in pancreatic alpha cells of diabetic and non-diabetic mice. Histochem Cell Biol 127, 227–232 (2007). https://doi.org/10.1007/s00418-006-0248-4

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  • DOI: https://doi.org/10.1007/s00418-006-0248-4

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