Lipid peroxidation as the mechanism of modification of brain 5?-nucleotidase activity in vitro

Mishra, Om P.; Delivoria‐Papadopoulos, Maria; Cahillane, G.; Wagerle, L Craig

doi:10.1007/bf00968666

Cited by 20 publications

(4 citation statements)

References 33 publications

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“…A decrease in intracellular ATP under oxidative stress may also result from its release and subsequent extracellular metabolization to adenosine by ectonucleotidases. These results are in agreement with our previous data obtained in cultured retinal neurons exposed to ascorbate/Fe 2ϩ (21,28) and with an increase in ecto-5Ј-nucleotidase activity observed after oxidation of brain membranes (34). However, we cannot exclude the contribution of reversal of the nucleoside transporter.…”

Section: Discussionsupporting

confidence: 93%

Insulin Restores Metabolic Function in Cultured Cortical Neurons Subjected to Oxidative Stress

et al. 2006

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We previously demonstrated that insulin has a neuroprotective role against oxidative stress, a deleterious condition associated with diabetes, ischemia, and age-related neurodegenerative diseases. In this study, we investigated the effect of insulin on neuronal glucose uptake and metabolism after oxidative stress in rat primary cortical neurons. On oxidative stress, insulin stimulates neuronal glucose uptake and subsequent metabolism into pyruvate, restoring intracellular ATP and phosphocreatine. Insulin also increases intracellular and decreases extracellular adenosine, counteracting the effect of oxidative stress. Insulin effects are apparently mediated by phosphatidylinositol 3-K and extracellular signal-regulated kinase signaling pathways. Extracellular adenosine under oxidative stress is largely inhibited after blockade of ecto-5-nucleotidase, suggesting that extracellular adenosine results preferentially from ATP release and catabolism. Moreover, insulin appears to interfere with the ATP release induced by oxidative stress, regulating extracellular adenosine levels. In conclusion, insulin neuroprotection against oxidative stress-mediated damage involves 1) stimulation of glucose uptake and metabolism, increasing energy levels and intracellular adenosine and, ultimately, uric acid formation and 2) a decrease in extracellular adenosine, which may reduce the facilitatory activity of adenosine receptors.

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Section: Discussionsupporting

confidence: 93%

Insulin Restores Metabolic Function in Cultured Cortical Neurons Subjected to Oxidative Stress

et al. 2006

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“…Both enzymes are reported to be responsible for adenosine production.2324 Because the active site of the ecto-5'-nucleotidase faces the extracellular space, this enzyme is susceptible to extracellular free radicals. 25 This evidence may lead us to support the view that SOD administration may preserve ecto-5'-nucleotidase activity and increase adenosine production in coronary microembolization.…”

supporting

confidence: 60%

Superoxide dismutase restores contractile and metabolic dysfunction through augmentation of adenosine release in coronary microembolization.

et al. 1993

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Background. This study was undertaken to test the hypothesis that administration of superoxide dismutase (SOD) restores the contractile and metabolic dysfunction in coronary microembolization and that these beneficial effects of SOD are attributable to the restoration of 5'-nucleotidase activity and subsequent augmentation of adenosine release.Methods and Results. In 78 dogs before and after an injection of microspheres (15 pm in diameter) into the left anterior descending coronary artery, regional coronary blood flow (CBF), fractional shortening (FS), and lactate extraction ratio (LER) were measured with and without administration of recombinant human SOD (50 ,g/kg/min i.c.). In the untreated dogs (n=6), both FS and LER decreased after coronary microembolization (2.0x10' microspheres per ml CBF [mLIminJ). FS and LER decreased from 24.2±13% to 5.1±1.2% and from 23.0+1.1% to -10.5+2.9%o, respectively. These ischemic changes were associated with coronary hyperemic flow (141±8 versus 92±1 mL/100 g/min) and adenosine release (5.8±0.5 versus 0.4±0.1 nmol/100 g/min). Pretreatment with SOD augmented the hyperemic flow to 164±4 mVJ100 g/min and enhanced the release of adenosine (9.6±0.6 nmol/100 g/min) associated with improvement of functional and metabolic dysfunction (FS, 14.8+2.3%; LER, 15.1±3.1%). Administration of SOD at 10 minutes (n=5) and 30 minutes (n=5) after coronary embolization restored the contractile function and lactate metabolism (at 10 minutes: FS, 16.7±2.2% and LER, 16.7±3.9%o; at 30 minutes: FS, 11.1±1.3% and LER, 7.2±3.1%). However, administration of SOD 60 minutes after coronary embolization (n=6) did not restore the contractile and metabolic dysfunction. The restoration of the contractile and metabolic dysfunction by SOD treatment was blunted by adenosine receptor blockade with 8-phenyltheophylline (n=5). Myocardial 5'-nucleotidase activity at 2 hours after embolization was restored with SOD treatment at 10 minutes (n=5) and 30 minutes (n=5) after embolization. However, SOD treatment at 60 minutes after embolization (n=6) did not restore 5'-nucleotidase activity compared with the SOD pretreatment group. Furthermore, coronary submaximal vasodilation induced by papaverine (n=5) and adenosine (n=5) abolished the beneficial effects of SOD.Conclusions. We conclude that 1) in sustained myocardial ischemia, SOD treatment attenuates ischemic injury caused by coronary microembolization by restoration of 5'-nucleotidase activity and augmentation of adenosine release; 2) this beneficial effect of SOD is observed even after coronary microembolization; and 3) the beneficial effects of SOD are attributable to coronary vasodilation produced by augmented adenosine release. (Circulation 1993;87:982-995 To test the hypothesis that SOD restores contractile and metabolic dysfunction after the onset of coronary microembolization, we administered SOD before and 10, 30, 60, and 120 minutes after embolization of microspheres. We also determined whether the beneficial effects of SOD are attributable to coronary vasodilati...

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“…The FeCl 2 /VC system has been widely used to induce oxidative damage in in vitro experiments, producing free radicals [22,23]. We have used a fluorescence spectrometric assay to detect the generation of ROS in this system.…”

Section: Discussionmentioning

confidence: 99%

“…Brain was removed for immediate mitochondrial isolation [20,21]. Oxidative brain mitochondrial damage was induced with FeCl 2 /VC and measured with the thiobarbituric acid method [22,23].…”

Section: Mitochondrial Preparation and Fecl 2 /Ascorbic Acid (Vc)-stimentioning

confidence: 99%

A Milk-Based Wolfberry Preparation Prevents Prenatal Stress-Induced Cognitive Impairment of Offspring Rats, and Inhibits Oxidative Damage and Mitochondrial Dysfunction In Vitro

Feng

Jia

et al. 2010

Neurochem Res

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Lycium barbarum (Fructus Lycii, Wolfberry, or Gouqi) belongs to the Solanaceae. The red-colored fruits of L. barbarum have been used for a long time as an ingredient in Chinese cuisine and brewing, and also in traditional Chinese herbal medicine for improving health. However, its effects on cognitive function have not been well studied. In the present study, prevention of a milk-based wolfberry preparation (WP) on cognitive dysfunction was tested in a prenatal stress model with rats and the antioxidant mechanism was tested by in vitro experiments. We found that prenatal stress caused a significant decrease in cognitive function (Morris water maze test) in female offspring. Pretreatment of the mother rats with WP significantly prevented the prenatal stress-induced cognitive dysfunction. In vitro studies showed that WP dose-dependently scavenged hydroxyl and superoxide radicals (determined by an electron spin resonance spectrometric assay), and inhibited FeCl(2)/ascorbic acid-induced dysfunction in brain tissue and tissue mitochondria, including increases in reactive oxygen species and lipid peroxidation and decreases in the activities of complex I, complex II, and glutamate cysteine ligase. These results suggest that dietary supplementation with WP may be an effective strategy for preventing the brain oxidative mitochondrial damage and cognitive dysfunction associated with prenatal stress.

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Lipid peroxidation as the mechanism of modification of brain 5?-nucleotidase activity in vitro

Cited by 20 publications

References 33 publications

Insulin Restores Metabolic Function in Cultured Cortical Neurons Subjected to Oxidative Stress

Insulin Restores Metabolic Function in Cultured Cortical Neurons Subjected to Oxidative Stress

Superoxide dismutase restores contractile and metabolic dysfunction through augmentation of adenosine release in coronary microembolization.

A Milk-Based Wolfberry Preparation Prevents Prenatal Stress-Induced Cognitive Impairment of Offspring Rats, and Inhibits Oxidative Damage and Mitochondrial Dysfunction In Vitro

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