Stress proteins and oxidative damage in a renal derived cell line exposed to inorganic mercury and lead

Stacchiotti, Alessandra; Morandini, Fausta; Bettoni, Francesca; Schena, Ilaria; Llombart‐Bosch, Antonio; Grigolato, Pier Giovanni; Apostoli, Pietro; Rezzani, Rita; Aleo, Maria Francesca

doi:10.1016/j.tox.2009.08.014

Cited by 94 publications

(50 citation statements)

References 52 publications

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“…The appearance of α-GST in urine is thought to result from the leakage of cytosolic contents when proximal tubule epithelial cells die Vaidya et al, 2008). Up-regulation of GSTs mRNA in our study was concomitant with a previous study which demonstrated activation of this enzyme after mercury and lead treatment (Stacchiotti et al, 2009). …”

Section: Discussionsupporting

confidence: 91%

“…It has been demonstrated that heavy metals share common primary mechanisms of toxicity, including oxidative (Stacchiotti et al, 2009). Renal toxicity commonly occurs after administration of xenobiotics, including heavy metals.…”

Section: Discussionmentioning

confidence: 99%

“…Most genes in this category were glutathione-S-transferases (GSTs). GSTs are three enzyme families with different subcellular locations that detoxify noxious xenobiotics and protect against reactive compounds produced during oxidative stress (Stacchiotti et al, 2009). During GST-mediated reactions, glutathione (GSH) is conjugated with various electrophiles or oxidation end product and the GSH adducts are actively secreted by the cell.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Mercuric Chloride on Gene Expression in NRK-52E Cells

Ahn¹,

Baik²,

Ko³

et al. 2010

Genomics & Informatics

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Mercuric chloride, a model nephrotoxicant was used to elucidate time-and dose-dependent global gene expression changes associated with proximal tubular toxicity. Rat kidney cell lines NRK-52E cells were exposed for 2, 6 and 12 hours and with 3 different doses of mercuric chloride. Cell viability assay showed that mercuric chloride had toxic effects on NRK-52E cells causing 20% cell death (IC20) at 40μM concentration. We set this IC20 as high dose concentration and 1/5 and 1/25 concentration of LC20 were used as mid and low concentration, respectively. Analyses of microarray data revealed that 738 genes were differentially expressed (more than two-fold change and p＜0.05) by low concentration of mercuric chloride at least one time point in NRK-52E cells. 317 and 2,499 genes were differentially expressed at mid and high concentration of mercuric chloride, respectively. These deregulated genes showed a primary involvement with protein trafficking (CAV2, CANX, CORO1B), detoxification (GSTs) and immunity and defense (HMOX1, NQO1). Several of these genes were previously reported to be up-regulated in proximal tubule cells treated with nephrotoxicants and might be aid in promoting the predictive biomarkers for nephrotoxicity.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effects of Mercuric Chloride on Gene Expression in NRK-52E Cells

Ahn¹,

Baik²,

Ko³

et al. 2010

Genomics & Informatics

View full text Add to dashboard Cite

show abstract

“…Based on our knowledge, it is well known that lead exposure increases the occurrence of cell death via apoptosis, such as neural (Suresh et al, 2006;Chetty et al, 2007), renal (Stacchiotti et al, 2009) and testicular cells (Adhikari et al, 2001;Massanyi et al, 2007). The cellular toxic effect of lead may be mediated by apoptosis.…”

Section: Discussionmentioning

confidence: 98%

Overexpression of Ref-1 Inhibits Lead-induced Endothelial Cell Death via the Upregulation of Catalase

Lee

Kim

et al. 2009

Korean J Physiol Pharmacol

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“…When cells were exposed to various stimuli, such as heat, cold, or heavy metal stress, GRP78 overexpression immediately resulted in cell recovery and cell protection against stress (Luan et al, 2009;Stacchiotti et al, 2009). The upregulation of stress proteins is an important step for inhibiting protein aggregation and misfolding following stress (Richter-Landberg and Goldbaum, 2003).…”

Section: Discussionmentioning

confidence: 99%

Association analysis between SNPs in the 5'-flanking region of the chicken GRP78 gene, thermotolerance parameters, and tissue mRNA expression

Kong¹,

Zhang²,

Ji³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Glucose-regulated protein 78 (GRP78) is a molecular chaperone in the endoplasmic reticulum and can be induced by different kinds of environmental and physiological stress. Thus far, the role of the GRP78 gene in thermotolerance in chickens has not been investigated. In the present study, we detected sequence variations in the 5ꞌ-flanking region of the GRP78 gene and evaluated several thermotolerance parameters, such as T3, corticosterone, H/L ratio, and levels of CD3 + , CD4 + , and CD8 + T cells, to further determine its associations at 35° and 15°C. The sequencing results revealed 10 SNPs in the 5'-flanking region of the GRP78 gene, and seven mutations were chosen for further genotyping in a White Recessive Rock (WRR) chicken population. The SNP C.-744C>G in WRR chickens was significantly correlated with heat tolerance parameters under both conditions; it may therefore exert 6111 Chicken GRP78 gene expression and thermotolerance ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 6110-6123 (2015) a potential hereditary effect on heat tolerance, and the genotype GG may be advantageous for thermotolerance. The heart, liver, brain, and leg muscle tissues of 8-day-old WRR chickens were sampled from heat stress groups, which were defined by exposure to 1, 2, 3, and 6 h of persistent thermal stress, and a control group, which was not exposed to thermal stress. Quantitative real-time polymerase chain reaction assay indicated that the mRNA expression level of the GRP78 gene increased gradually under heat stress, peaked at 3 h, and then decreased. We conclude that the mRNA expression of the GRP78 gene is time-and tissue-dependent.

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Stress proteins and oxidative damage in a renal derived cell line exposed to inorganic mercury and lead

Cited by 94 publications

References 52 publications

Effects of Mercuric Chloride on Gene Expression in NRK-52E Cells

Effects of Mercuric Chloride on Gene Expression in NRK-52E Cells

Overexpression of Ref-1 Inhibits Lead-induced Endothelial Cell Death via the Upregulation of Catalase

Association analysis between SNPs in the 5'-flanking region of the chicken GRP78 gene, thermotolerance parameters, and tissue mRNA expression

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