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Alloxan

About: Alloxan is a research topic. Over the lifetime, 6194 publications have been published within this topic receiving 111216 citations. The topic is also known as: NSC 7169 & 5,6-dioxouracil.


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Journal ArticleDOI
TL;DR: It is considered that, unlike free fatty acid, triglyceride fatty acid which accumulates in the livers of normal, fed rats is oxidized slowly, and that glucagon may not exert a major ketogenic action by stimulation of a hepatic triglyceride lipase.

267 citations

Journal ArticleDOI
TL;DR: The results suggest that the activation of retinal NF-κB in diabetes is an early event in the development of retinopathy, and it remains active when the retinal capillary cell death is accelerating, and histopathology is developing.
Abstract: Oxidative stress is increased in the retina in diabetes, and long-term administration of antioxidants inhibits the development of retinopathy in diabetic rats. The purpose of this study is to determine how diabetes affects the activation of a redox-sensitive nuclear transcriptional factor in the retina, NF-κB, and its inhibition by antioxidants. Alloxan diabetic rats were assigned to receive standard diet or the diet supplemented with multiple antioxidants, including ascorbic acid, Trolox, dl α-tocopherol acetate, N-acetyl cysteine, β-carotene, and selenium for up to 14 months. NF-κB activation, oxidative stress and nitric oxides were measured in the retina at 2, 8 and 14 months of diabetes. Retinal NF-κB was activated by about 60% at two months after induction of diabetes, remained activated for up to 14 months of diabetes, and the duration of diabetes had no effect on the intensity of NF-κB activation. Similarly, oxidative stress and nitric oxides were elevated by over 50% in the retina of rats diabetic...

266 citations

Journal ArticleDOI
TL;DR: Berberine significantly inhibited the progression of diabetes induced by alloxan, and the inhibitory effect of berberine on diabetes might be associated with its hypoglycemic effect, modulating lipids metabolic effects and its ability to scavenge free radical.

262 citations

Journal ArticleDOI
TL;DR: Human beta cells are resistant to NP, SZ, or alloxan at concentrations that decrease survival and function of rat or mouse beta cells, raising the possibility that such differences may also be present among individuals of the same species.
Abstract: The ability of beta cells to endure assaults may be relevant in the development of insulin-dependent diabetes mellitus. This study examines the susceptibility of human pancreatic islets to agents that are cytotoxic for rodent beta cells--i.e., sodium nitroprusside (NP, a nitric oxide donor), streptozotocin (SZ), or alloxan. After 5-8 days in tissue culture, human or rodent islets were exposed for 14 h to NP (50-200 microM) or for 30 min to SZ or alloxan (1-3 mM). Glucose oxidation by human islets was not reduced by NP, but there was a dose-dependent inhibition in rat (40-90% inhibition; P < 0.001) and mouse (10-60% inhibition; P < 0.05) islet glucose oxidation. Glucose (16.7 mM)-induced insulin release by human islets was not impaired after a 30-min exposure to SZ or alloxan, at concentrations that inhibited insulin release from rat (30-80% inhibition; P < 0.001) or mouse (10-70% inhibition; P < 0.05) islets. The viability of human beta cells purified by flow cytometry was not affected by SZ or alloxan (5 mM), as judged 1 or 4 days after a 10-min exposure and subsequent culture; these conditions were cytotoxic for rat beta cells, with 65-95% (P < 0.01) dead beta cells after 4 days. Human islets transplanted under the kidney capsule of nude mice were not affected by in vivo alloxan exposure, as suggested by preserved graft morphology and insulin content, whereas the endogenous beta cells of the transplanted mice were severely damage (80% decrease in pancreatic insulin content and morphological signs of beta-cell destruction). Thus human beta cells are resistant to NP, SZ, or alloxan at concentrations that decrease survival and function of rat or mouse beta cells. These marked interspecies differences emphasize the relevance of repair and/or defense mechanisms in beta-cell destruction and raise the possibility that such differences may also be present among individuals of the same species.

260 citations

Journal ArticleDOI
TL;DR: The data of the present study are consistent with a role for the hydroxyl radical and appear to rule out a direct causative role for hydrogen peroxide, while other data rule out any protective role for transiently elevated levels of blood glucose resulting from the administered compounds.

252 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20241
2023116
2022330
2021108
2020192
2019188