Lead amplifies glutamate-induced oxidative stress

Naarala, Jonne; Loikkanen, Jarkko; Ruotsalainen, Marjo; Savolainen, Kai

doi:10.1016/0891-5849(95)00067-8

Cited by 54 publications

(18 citation statements)

References 28 publications

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“…This compound reacts quantitatively with oxygen species within the cell to produce the fluorescent dye 2',7'-dichlorofluorescein (DCF), which remains trapped within the cell and can be measured as an index of intracellular oxidation. All experiments were performed in the presence of diethyl maleate (0.02%) in the medium, to lower intracellular glutathione levels (Naarala et al 1995).…”

Section: Methodsmentioning

confidence: 99%

U-83836E prevents kainic acid-induced neuronal damage

Camins

Gabriel

Aguirre

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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The effect of kainic acid (KA) on mitochondrial membrane potential (MMP) and reactive-oxygen species (ROS) production was studied in dissociated cerebellar granule cells from rat pups. KA induced a maximum increase of 361%+/-35% in ROS production. The lazaroid compound U-83836E (at concentrations ranging from 10(-9) to 5x10(-6) M) completely inhibited this increase, with an IC50 value of 3.02+/-1.08x10(-7) M. KA also decreased the mitochondrial membrane potential (MMP), with a maximum decrease of about 30%. Absence of Na+ in the incubation medium did not significantly alter the effect of KA on MMP. As expected, the AMPA/kainate receptor antagonist NBQX inhibited the effects of KA on MMP with an IC50 value of 1.1+/-0.8 microM. However, the lazaroid U-83836E, indomethacin, nor-dihydroguaiaretic acid and L-nitroarginine all failed to inhibit the KA-induced decrease in the MMP. Finally, to assess the neuroprotective effect of U-83836E on KA-induced neurotoxicity in vivo, the increase in the peripheral-type benzodiazepine receptor density in rat hippocampus was measured. Treatment with KA increased the Bmax to 1341+/-192 fmol mg(-1). When U-83836E was coadministered with KA, the Bmax was reduced to 765+/-122 fmol mg(-1), which was not significantly different from the Bmax obtained from untreated rats (Bmax: 518+/-33 fmol mg(-1)). We conclude that treatment with the lazaroid U-83836E might be a suitable therapeutic strategy in neurodegenerative disorders.

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Section: Methodsmentioning

confidence: 99%

U-83836E prevents kainic acid-induced neuronal damage

Camins

Gabriel

Aguirre

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Digitonin was used for demolishing cell membrane integrity. This enables PI to enter all cells, allowing calculation of viability from the relative PI value before and after the addition of digitonin [26]. The maximum PI fluorescence value (after digitonin treatment) reflects the number of cells, and also enabled possible intergroup differences in cell count to be checked (due to, e.g.…”

Section: Viability Of Cellsmentioning

confidence: 99%

Induction of micronuclei and superoxide production in neuroblastoma and glioma cell lines exposed to weak 50 Hz magnetic fields

Kesari¹,

Juutilainen²,

Luukkonen³

et al. 2016

J. R. Soc. Interface.

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Extremely low-frequency (ELF) magnetic fields (MF) have been associated with adverse health effects in epidemiological studies. However, there is no known mechanism for biological effects of weak environmental MFs. Previous studies indicate MF effects on DNA integrity and reactive oxygen species, but such evidence is limited to MFs higher (greater than or equal to 100 mT) than those generally found in the environment. Effects of 10 and 30 mT fields were studied in SH-SY5Y and C6 cells exposed to 50-Hz MFs for 24 h. Based on earlier findings, menadione (MQ) was used as a cofactor. Responses to MF were observed in both cell lines, but the effects differed between the cell lines. Micronuclei were significantly increased in SH-SY5Y cells at 30 mT. This effect was largest at the highest MQ dose used. Increased cytosolic and mitochondrial superoxide levels were observed in C6 cells. The effects on superoxide levels were independent of MQ, enabling further mechanistic studies without co-exposure to MQ. The micronucleus and mitochondrial superoxide data were consistent with a conventional rising exposure -response relationship. For cytosolic superoxide, the effect size was unexpectedly large at 10 mT. The results indicate that the threshold for biological effects of ELF MFs is 10 mT or less.

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“…It also amplifies oxidative stress induced by l-glutamate [14] . Recent studies suggest that accumulated lead exposure is related to several chronic disorders of aging including disorders that have been associated with oxidative stress [15][16][17] . Sass [19] first reported that lead poisoning in dogs is associated with perforating gastrointestinal ulcers.…”

Section: Introductionmentioning

confidence: 99%

Lead exposure increases oxidative stress in the gastric mucosa of HCl/ethanol-exposed rats

Olaleye

Adaramoye²,

.³

et al. 2007

WJG

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AIM:To investigate the role of reactive oxygen species in the ulcer-aggravating effect of lead in albino rats. METHODS:Albino Wistar rats were randomly divided into three groups and treated orally with 100 mg/L (low dose) or 5000 mg/L (high dose) of lead acetate for 15 wk. A third group received saline and served as control. At the end of wk 15, colorimetric assays were applied to determine the concentrations of total protein and nitrite, the activities of the oxidative enzymes catalase and superoxide dismutase, and lipid peroxidation in homogenized gastric mucosal samples. RESULTS:Exposure of rats to lead significantly increased the gastric mucosal damage caused by acidified ethanol. Although the basal gastric acid secretory rate was not significantly altered, the maximal response of the stomach to histamine was significantly higher in the lead-exposed animals than in the unexposed control group. Exposure to low and high levels of lead significantly increased gastric lipid peroxidation to 183.2% ± 12.7% and 226.1% ± 6.8% of control values respectively (P < 0.0). On the other hand, lead exposure significantly decreased catalase and superoxide dismutase (SOD) activities and the amount of nitrite in gastric mucosal samples. CONCLUSION:Lead increases the formation of gastric ulcers by interfering with the oxidative metabolism in the stomach.

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Lead amplifies glutamate-induced oxidative stress

Cited by 54 publications

References 28 publications

U-83836E prevents kainic acid-induced neuronal damage

U-83836E prevents kainic acid-induced neuronal damage

Induction of micronuclei and superoxide production in neuroblastoma and glioma cell lines exposed to weak 50 Hz magnetic fields

Lead exposure increases oxidative stress in the gastric mucosa of HCl/ethanol-exposed rats

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