作者: Mohamed S. Abdel-Rahman , Fatma I. Elrakhawy , Fakhry A. Iskander
DOI: 10.1016/0378-4274(92)90007-7
关键词: Superoxide dismutase 、 Internal medicine 、 Degranulation 、 Biology 、 Insulin 、 Mitochondrion 、 Alloxan 、 Pancreas 、 Islet 、 Endocrinology 、 Toxicity
摘要: Abstract Alloxan induces diabetes in laboratory animals through the destruction of endocrine pancreatic B cells. The mechanism alloxan toxicity is still obscure. This study was conducted to investigate effects Superoxide dismutase (SOD) or reduced nicotinamide adenine dinucleotide (NADPH) treatment on cells isolated rat islets prior treatment. Islets were treated with SOD (1000 U) 0.1 mM NADPH for 10 min followed by (0.18 mg) 5 min. Insulin secretion studied samples incubated 60 media supplemented glucose (1.8 mg ml ). Morphological examinations fixed after significantly protected from cytotoxic effect alloxan. Although decreased insulin 35% control, increased this level 73% control values. did not provide any protection islets. and different that alone. changes observed alone presence NADPH. exhibited multiple cellular necrosis, marked degranulation extensive vesiculation endoplasmic reticulum Golgi complex. Mitochondrial enlargement disrupted cristae mitochondrial ruptures prominent. However, similar except enlarged mitochondria. reinforces free radical hypothesis toxicity. markedly mitochondria one targets which destroyed