Effects of glucose concentration on redox status in rat primary cortical neurons under hypoxia

Shi, Honglian; Liu, Ke Jian

doi:10.1016/j.neulet.2006.09.066

Cited by 43 publications

(37 citation statements)

References 30 publications

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“…Intracellular ROS and hydroxyl radical accumulation induced lipid peroxidation (LPO) (30); thus, lipid molecules were consumed uninterruptedly, decreasing the amount of unsaturated fatty acid and affecting the fluidity of biological membranes (31). MG and other aldehydes react with proteins and enzymes, which cause them to lose their biological activity and lead to an abnormal metabolism.…”

Section: Discussionmentioning

confidence: 99%

Formation of a salsolinol-like compound, the neurotoxin, 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, in a cellular model of hyperglycemia and a rat model of diabetes

Song

Xin

Xie

et al. 2013

International Journal of Molecular Medicine

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Abstract. There are statistical data indicating that diabetes is a risk factor for Parkinson's disease (PD). Methylglyoxal (MG), a biologically reactive byproduct of glucose metabolism, the levels of which have been shown to be increase in diabetes, reacts with dopamine to form 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (ADTIQ); this formation may provide further insight into the connection between PD and diabetes. In this study, we investigated the role of ADTIQ in these two diseases to determine in an aim to enhance our understanding of the link between PD and diabetes. To this end, a cell model of hyperglycemia and a rat model of diabetes were established. In the cell model of hyperglycemia, compared with the control group, the elevated glucose levels promoted free hydroxyl radical formation (p<0.01). An ADTIQ assay was successfully developed and ADTIQ levels were detected and quantified. The levels of its precursors, MG and dopamine (DA), were determined in both the cell model of hyperglycemia and the rat model of diabetes. The proteins related to glucose metabolism were also assayed. Compared with the control group, ADTIQ and MG levels were significantly elevated not only in the cell model of hyperglycemia, but also in the brains of rats with diabetes (p<0.01). Seven key enzymes from the glycolytic pathway were found to be significantly more abundant in the brains of rats with diabetes. Moreover, it was found that adenosine triphosphate (ATP) synthase and superoxide dismutase (SOD) expression levels were markedly decreased in the rats with diabetes compared with the control group. Therefore, ADTIQ expression levels were found to be elevated under hyperglycemic conditions. The results reported herein demonstrate that ADTIQ, which is derived from MG, the levels of which areincreased in diabetes, may serve as a neurotoxin to dopaminergic neurons, eventually leading to PD. IntroductionDiabetes mellitus (DM), as a state of chronic hyperglycemia, and Parkinson's disease (PD) are diseases which consist a global health threat. In recent years, there have been increasing data indicating that hyperglycemia is associated with an increased risk of developing PD (1,2). However, the mechanisms underlying the association between hyperglycemia and PD have not yet been elucidated.Deng and Rajput (6) were the first to report, in 2001, that 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (ADTIQ), a salsolinol-like compound, is found at highly concentrated levels in the brains of patients who suffer from PD (3). When the brains of deceased patients with PD were compared to those of normal subjects, it was found that patients with PD presented elevated levels of ADTIQ in all the examined brain areas. This finding indicated that elevated ADTIQ expression levels may be one of the mechanisms involved in the increased risk patients with diabetes have of developing PD (4).Formation of a salsolinol-like compound, the neurotoxin, 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, in a cellular model of hyperglycem...

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Section: Discussionmentioning

confidence: 99%

Formation of a salsolinol-like compound, the neurotoxin, 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, in a cellular model of hyperglycemia and a rat model of diabetes

Song

Xin

Xie

et al. 2013

International Journal of Molecular Medicine

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“…Interestingly, both glucose deprivation and high glucose exposure have been shown to be toxic to cells. Incubating with elevated glucose levels can also induce neuronal death in PC12 cells (Shi and Liu 2006).…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that glucose deprivation causes perturbations in cellular sensitivity to oxidative stress, which is mediated by increased generation of pro-oxidants and decreased scavenging of free radicals. In primary dorsal root ganglion neurons, glucose (45 mM) rapidly induces a rise in ROS, and the toxicity induced by high glucose is blocked by inhibiting ROS induction (Shi and Liu 2006). However, no detailed study has been carried out to evaluate the inhibitory effect of saffron on high glucose-induced neurotoxicity in PC12 cells as an in vitro model for diabetic neuropathy.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Saffron Extract and Crocin on Reactive Oxygen Species-Mediated High Glucose-Induced Toxicity in PC12 Cells

2009

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Diabetic neuropathy is one of the most frequent complications of diabetes. Despite some studies, the exact mechanism of glucose neurotoxicity has not been fully elucidated. Increased reactive oxygen species (ROS) has proposed as a possible mechanism. Crocus sativus L. (saffron) has been known as a source of antioxidants. Therefore, neuroprotective effect of saffron extract, its active component crocin and gamma-glutamylcysteinylglycine (GSH) was studied in glucose-induced neurotoxicity, using PC12 cells as a suitable in vitro model of diabetic neuropathy. Cell viability was quantitated by MTT assay. ROS was measured using DCF-DA by flow cytometry analysis. The result showed that glucose (13.5 and 27 mg/ml) reduced the cell viability of PC12 cells after 4 days. Saffron extract (5 and 25 mg/ml), crocin (10 and 50 muM) and GSH (10 muM) could decrease this toxicity. Glucose toxicity was consistent with increased ROS production which reduced by saffron, crocin and GSH pretreatment. These results suggest saffron and its carotenoid crocin could be potentially useful in diabetic neuropathy treatment.

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“…Diversos estudos in vivo e in vitro demonstraram que a hiperglicemia a curto prazo protege miócitos cardíacos e neurônios [45][46][47] . .…”

Section: S132unclassified

Glycemic control and insulin therapy in sepsis and critical illness

et al. 2007

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Objetivo: Revisar a literatura sobre a fisiopatologia de hiperglicemia e controle glicêmico em crianças e adultos com sepse e doença crítica. Fontes de dados:Pesquisa não sistemática da literatura médica através da base de dados MEDLINE usando os termos hiperglicemia, controle glicêmico, terapia insulínica intensiva, sepse e terapia intensiva. Os artigos foram selecionados de acordo com sua relevância, conforme a opinião dos autores. Síntese dos dados:A hiperglicemia é freqüente em crianças com doenças críticas e está associada a desfecho negativo. Em adultos, não há um consenso sobre a eficácia e segurança do controle glicêmico. Descrevemos os possíveis mecanismos envolvidos em toxicidade da glicose e os efeitos benéficos do controle glicêmico. Estudos iniciais demonstraram que o uso de insulina para atingir controle glicêmico reduziu a morbimortalidade em terapia intensiva em adultos; no entanto, estudos recentes não confirmaram esses achados. É importante destacar que o controle glicêmico está evidentemente associado a aumento da incidência de hipoglicemia. A eficácia do controle glicêmico ainda não foi estudada em crianças criticamente doentes. Conclusão:O controle glicêmico é uma nova opção terapêutica em terapia intensiva. Evidências conflitantes em adultos significam que, antes de aplicar esta abordagem em pediatria, é necessário avaliá-la em ensaio clínico.J Pediatr (Rio J). 2007;83(5 Supl):S128-136: Hiperglicemia, controle glicêmico, nível de glicose, terapia insulínica, terapia intensiva, pediatria.Objective: To review the literature about the pathophysiology of hyperglycemia and glycemic control in children and adults with sepsis and critical illness.Sources: Non-systematic survey of the medical literature using MEDLINE and terms hyperglycemia, glycemic control, intensive insulin therapy, sepsis and intensive care. Articles were selected according to their relevance based on the authors' opinion. Summary of the findings:Hyperglycemia is frequent in critically ill children and it is associated with worsened outcome. In adults, there is no consensus on the efficacy and safety of glycemic control. We describe the possible mechanisms involved in glucose toxicity and the beneficial effects of glycemic control. Initial studies showed that use of insulin to achieve glycemic control reduced morbidity and mortality in adult intensive care; however, recent studies have failed to confirm these findings. Importantly, it is evident that glycemic control is associated with increased incidence of hypoglycemia. The efficacy of glycemic control has not yet been studied in critically ill children. Conclusion:Glycemic control is a novel therapeutic option in critical care. Conflicting evidence in adults means that before we apply this approach to pediatrics it will need to be assessed in clinical trial.J Pediatr (Rio J). 2007;83(5 Suppl):S128-136: Hyperglycemia, glycemic control, glucose level, insulin therapy, intensive care, pediatric. IntroduçãoO metabolismo de carboidratos é essencial para a sobrevivência. A escasse...

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Effects of glucose concentration on redox status in rat primary cortical neurons under hypoxia

Cited by 43 publications

References 30 publications

Formation of a salsolinol-like compound, the neurotoxin, 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, in a cellular model of hyperglycemia and a rat model of diabetes

Formation of a salsolinol-like compound, the neurotoxin, 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, in a cellular model of hyperglycemia and a rat model of diabetes

Protective Effect of Saffron Extract and Crocin on Reactive Oxygen Species-Mediated High Glucose-Induced Toxicity in PC12 Cells

Glycemic control and insulin therapy in sepsis and critical illness

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