Increase in intracellular Cd2+ concentration of rat cerebellar granule neurons incubated with cadmium chloride: Cadmium cytotoxicity under external Ca2+-free condition

Nishimura, Yumiko; Yamaguchi, Junya; Kanada, Aimi; Horimoto, Kanna; Kanemaru, Kaori; Satoh, Masaya; Oyama, Yasuo

doi:10.1016/j.tiv.2005.06.006

Cited by 43 publications

(19 citation statements)

References 32 publications

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“…CRHSP24 has been suggested to be involved in calcium-mediated signal transduction (39). As cadmium has been reported to interfere with calcium homeostasis in nerve cells (23)(24)(25), we suggest that PIPPin might be a novel and central target of cadmium action in the brain. …”

Section: Discussionmentioning

confidence: 79%

“…Cadmium enters the central nervous system either through the olfactory pathway or by altering the permeability of the blood-brain barrier (18)(19)(20)(21), and has been reported to cause lipid peroxidation (15), damage to DNA (22), and alteration of calcium homeostasis (23)(24)(25). Cadmium was also demonstrated to affect metabolism, release and re-uptake of different neurotransmitters (26)(27)(28)(29).…”

Section: Introductionmentioning

confidence: 99%

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The effect of cadmium on brain cells in culture

Gerspacher

Scheuber²,

Schiera³

et al. 2009

Int J Mol Med

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Abstract. Cadmium is a long-living heavy metal, abundantly present in the environment, which accumulates in the body. In this study, we investigated the effects of cadmium on the expression of molecular chaperones, and of certain cell-specific proteins, in a variety of brain cell types in culture, namely primary cultures of rat cortical neurons and astrocytes, a brain capillary endothelial cell line (RB4E.B cells), and pheochromocytoma cells (PC12), induced or not to differentiate by NGF treatment. The metal induces a dose-dependent increase of Hsp70 in all cell types. Responses to the metal are cellspecific in the case of Hsc70 and Hsp90: i) in astrocytes, as well as in PC12 cells, cadmium has no significant effect; ii) in endothelial cells, an increase of both proteins is clearly observable from 20 μM cadmium; iii) both Hsp90 and Hsc70 decrease in neurons treated with high doses of cadmium. Damage to the cytoskeleton in treated cells was also evident. Finally, we report that the metal at high doses induces a decrease of PIPPin (also known as CSD-C2), a putative RNAbinding protein highly expressed in neurons and probably involved in the regulation of histone replacement variant expression.

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Section: Discussionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

The effect of cadmium on brain cells in culture

Gerspacher

Scheuber²,

Schiera³

et al. 2009

Int J Mol Med

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“…In adult rats exposed to Cd, there was an increase of LP in the corpus striatum and cerebral cortex (Pal et al, 1993). (Nishimura et al, 2006) reported that Cd can enter the brain parenchyma and neurons and causes neurological alterations in humans (Rose et al, 1992) and animal models (Lukawski et al, 2005), leading to lower attention, hyper nociception, and olfactory dysfunction and memory deficits.…”

Section: Discussion:-mentioning

confidence: 99%

Ameliorating Effect of Vitamin-E Against Cadmium (Cd) Induced Brain Oxidative Damage in Albino Rats.

BhuvaneswariDevi¹,

KiranKumari²

2017

IJAR

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Acute exposure to moderately high concentrations of freshly generated cadmium oxide fumes (200-500 µg cadmium/m 3 ) may cause symptoms like the metal fume fever. The present study addressed the effect of Cadmium (Cd) on Oxidative Stress in rat brain. The three months rats were exposed to Cd intraperitonially at concentrations of low dose (1.5mg/kg bw) and high dose (3mg/kg bw) for a period of three weeks. A separate batch of low dose and high dose of Cd exposed rats received Vitamin-E intraperitonially for a week. In this study, we have examined the Glutathione peroxidase (GPX) activity, Glutathione reductase (GR) activity, Glutathione-stransferase (GST) activity, Xanthine oxidase (XO) activity levels and Lipid peroxidation (LP) in three brain regions, Cerebral Cortex, Cerebellum, and Hippocampus. We assessed the biochemical end points indicative of oxidative Stress in these three brain regions. The GPX, GR, and XO activity levels showed significant decrease and the GST activity, LP levels showed significant increase over control rats in dose dependent manner. The exposure to Vitamin-E however to low and high dose of Cd showed recovery, the GPX, GR, and XO activity levels were increased and decreased GST activity, Lipid Peroxidation were observed. The results may be attributed to the reason that the Cd exposure disrupts the functioning of brain which resulted in oxidative deficits. The Vitamin-E lessened the Cd burden in the brain as effective chelating agent decreasing the oxidative stress.

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“…Calcium imaging was performed as previously described [24,25]. Neurons were cultured in 3.5 cm plates at density 3 × 105 cells.…”

Section: Calcium Imagingmentioning

confidence: 99%

Neuroprotection of Sesamin against Cerebral Ischemia In-Vivo and N-Methyl-D-Aspartate-Induced Apoptosis In-Vitro

Tian¹,

Tian²

2015

Biochem Pharmacol (Los Angel)

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Increase in intracellular Cd2+ concentration of rat cerebellar granule neurons incubated with cadmium chloride: Cadmium cytotoxicity under external Ca2+-free condition

Cited by 43 publications

References 32 publications

The effect of cadmium on brain cells in culture

The effect of cadmium on brain cells in culture

Ameliorating Effect of Vitamin-E Against Cadmium (Cd) Induced Brain Oxidative Damage in Albino Rats.

Neuroprotection of Sesamin against Cerebral Ischemia In-Vivo and N-Methyl-D-Aspartate-Induced Apoptosis In-Vitro

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