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Título: | Pancreatic nitric oxide and oxygen free radicals in the early stages of streptozotocin-induced diabetes mellitus in the rat |
Autor: | González, Elida; Roselló-Catafau, Joan CSIC ORCID; Jawerbaum, Alicia; Sinner, Débora; Pustovrh, Carolina; Vela, J.; White, Verónica; Xaus, Carme CSIC; Peralta, Carmen; Gimeno, M. | Palabras clave: | Nitric oxide Oxidative stress Pancreas Streptozotocin diabetes |
Fecha de publicación: | 2000 | Editor: | Associação Brasileira de Divulgação Científica | Citación: | Brazilian Journal of Medical and Biological Research 33(11): 1335-1342 (2000) | Resumen: | The objective of the present study was to explore the regulatory mechanisms of free radicals during streptozotocin (STZ)-induced pancreatic damage, which may involve nitric oxide (NO) production as a modulator of cellular oxidative stress. Removal of oxygen species by incubating pancreatic tissues in the presence of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) (1 U/ml) produced a decrease in nitrite levels (42%) and NO synthase (NOS) activity (50%) in diabetic but not in control samples. When NO production was blocked by N(G)monomethyl-L-arginine (L-NMMA) (600 μM), SOD activity increased (15.21 ± 1.23 vs 24.40 ± 2.01 U/mg dry weight). The increase was abolished when the NO donor, spermine nonoate, was added to the incubating medium (13.2 ± 1.32). Lipid peroxidation was lower in diabetic tissues when PEG-SOD was added (0.40 ± 0.02 vs 0.20 ± 0.03 nmol/mg protein), and when L-NMMA blocked NOS activity in the incubating medium (0.28 ± 0.05); spermine nonoate (100 μM) abolished the decrease in lipoperoxide level (0.70 ± 0.02). We conclude that removal of oxygen species produces a decrease in pancreatic NO and NOS levels in STZ-treated rats. Moreover, inhibition of NOS activity produces an increase in SOD activity and a decrease in lipoperoxidation in diabetic pancreatic tissues. Oxidative stress and NO pathway are related and seem to modulate each other in acute STZ-induced diabetic pancreas in the rat. | URI: | http://hdl.handle.net/10261/114071 | Identificadores: | issn: 0100-879X |
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