Long-Term Exposure to Cadmium Causes Hepatic Iron Deficiency through the Suppression of Iron-Transport-Related Gene Expression in the Proximal Duodenum.

Cadmium (Cd) is an environmental pollutant that damages various tissues. Cd may cause a depletion of iron stores and subsequently an iron deficiency state in the liver. However, the molecular mechanism of decreased iron accumulation in the liver induced by long-term exposure to Cd is unknown.

Cadmium Toxicity Is Regulated by Peroxisome Proliferator-Activated Receptor δ in Human Proximal Tubular Cells.

Cadmium (Cd) is a toxic heavy metal that is widely present in the environment. Renal proximal tubule disorder is the main symptom of Cd chronic poisoning. Our previous study demonstrated that Cd inhibits the total activities of peroxisome proliferator-activated receptor (PPAR) transcription factors in human and rat proximal tubular cells.

Changes in DNA-binding activity of transcription factors in the kidney of mice exposed to cadmium.

Cadmium (Cd) is a toxic heavy metal, long-term exposure to which causes renal damage associated with disruption in gene expression. Transcription factors whose activities were altered in the kidneys of mice exposed to Cd for 3 months were assessed using protein/DNA-binding assays. Female C57BL/6J mice were exposed to 300 ppm Cd in the diet for 3 months.

Cadmium toxicity mediated by the inhibition of SLC2A4 expression in human proximal Tubule cells.

Cadmium (Cd) is an environmental contaminant that causes renal toxicity. We have previously demonstrated that Cd induces renal toxicity by altering transcriptional activities. In this study, we show that Cd markedly inhibited the activity of transcription factor MEF2A in HK-2 human proximal tubule cells, which generated significant cytotoxicity in the cells.

Cadmium induces iron deficiency anemia through the suppression of iron transport in the duodenum.

Cadmium (Cd) is an environmental contaminant that triggers toxic effects in various tissues such as the kidney, liver, and lung. Cd can also cause abnormal iron metabolism, leading to anemia. Iron homeostasis is regulated by intestinal absorption.

Transcription Factors and Downstream Genes in Cadmium Toxicity.

Cadmium (Cd) is a harmful heavy metal widely present in the environment which can cause severe kidney damage. The proximal tubular cells are the main target of renal Cd toxicity. The consequences of Cd cytotoxicity involve apoptosis and necrosis.

Effect of Metallothionein-III on Mercury-Induced Chemokine Gene Expression.

Mercury compounds are known to cause central nervous system disorders; however the detailed molecular mechanisms of their actions remain unclear. Methylmercury increases the expression of several chemokine genes, specifically in the brain, while metallothionein-III (MT-III) has a protective role against various brain diseases. In this study, we investigated the involvement of MT-III in chemokine gene expression changes in response to methylmercury and mercury vapor in the cerebrum and cerebellum of wild-type mice and MT-III null mice.

Glutathione has a more important role than metallothionein-I/II against inorganic mercury-induced acute renal toxicity.

Inorganic mercury is a harmful heavy metal that causes severe kidney damage. Glutathione (GSH), a tripeptide comprising L-glutamic acid, glycine and L-cysteine, and metallothionein (MT), a cysteine-rich and metal-binding protein, are biologically important protective factors for renal toxicity by inorganic mercury. However, the relationship between GSH and MT for the prevention of renal toxicity by inorganic mercury is unknown.

Effects of long-term cadmium exposure on urinary metabolite profiles in mice.

Cadmium (Cd) is a common environmental pollutant with known toxic effects on the kidney. Urinary metabolomics is a promising approach to study mechanism by which Cd-induced nephrotoxicity. The aim of this study was to elucidate the mechanism of Cd toxicity and to develop specific biomarkers by identifying urinary metabolic changes after a long-term of Cd exposure and with the critical concentration of Cd in the kidney.

Effect of gestational cadmium exposure on fetal growth, polyubiquitinated protein and monoubiqutin levels in the fetal liver of mice.

Cadmium (Cd) is an environmental pollutant present in contaminated water, food and soil. Cd adversely affects fetal development. We exposed pregnant mice to daily oral doses of 5 and 10 mg/kg Cd and examined fetal growth.

Identification of ARNT-regulated BIRC3 as the target factor in cadmium renal toxicity.

Cadmium (Cd) is an environmental contaminant that exhibits renal toxicity. The target transcription factors involved in Cd renal toxicity are still unknown. In this study, we demonstrated that Cd decreased the activity of the ARNT transcription factor, and knockdown of ARNT significantly decreased the viability of human proximal tubular HK-2 cells.

Different Regulation of p53 Expression by Cadmium Exposure in Kidney, Liver, Intestine, Vasculature, and Brain Astrocytes.

Chronic exposure to cadmium (Cd) is known to adversely affect renal function. Our previous studies indicated that Cd induces p53-dependent apoptosis by inhibiting gene expression of the ubiquitin-conjugating enzyme (Ube) 2d family in both human and rat proximal tubular cells. In this study, the effects of Cd on protein expression of p53 and apoptotic signals in the kidney and liver of mice exposed to Cd for 12 months were examined, as well as the effects of Cd on p53 protein levels and gene expression of the Ube2d family in various cell lines.

Accumulation of p53 via down-regulation of UBE2D family genes is a critical pathway for cadmium-induced renal toxicity.

Chronic cadmium (Cd) exposure can induce renal toxicity. In Cd renal toxicity, p53 is thought to be involved. Our previous studies showed that Cd down-regulated gene expression of the UBE2D (ubiquitin-conjugating enzyme E2D) family members.

Involvement of ubiquitin-coding genes in cadmium-induced protein ubiquitination in human proximal tubular cells.

Cadmium (Cd) is a toxic heavy metal with a long half-life in humans. It causes disorders of various tissue systems, including the kidney, and is associated with protein aggregation. Our previous study demonstrated Cd-induced suppression of the UBE2D gene family, one of the ubiquitin-conjugating enzyme families.

Alteration of DNA binding activity of transcription factors in NRK-52E rat proximal tubular cells treated with cadmium.

Cadmium is a toxic heavy metal that causes severe clinical symptoms in various tissues including the kidney. In this study, activities of transcription factors were measured to identify what type of transcription factor was affected by cadmium in rat proximal tubular cells (NRK-52E cells) using the protein/DNA binding assay. After treatment of NRK-52E cells with 5 µM CdCl2 for 3 hr, nuclear extracts were used for the protein/DNA binding assay.

Arsenic (+3 oxidation state) methyltransferase is a specific but replaceable factor against arsenic toxicity.

Inorganic metalloids, such as arsenic (As), antimony (Sb), selenium (Se), and tellurium (Te), are methylated in biota. In particular, As, Se, and Te are methylated and excreted in urine. The biomethylation is thought to be a means to detoxify the metalloids.

Gene expression differences in the duodenum of 129/Sv and DBA/2 mice compared with that of C57BL/6J mice.

We compared the cadmium (Cd) concentration in the liver and kidney of different strains of mice after exposure to 50 ppm Cd for 30 days via drinking water. Cd concentration in the liver and kidney of C57BL/6J mice were higher than those of 129/Sv and DBA/2 mice. Since orally ingested heavy metals are absorbed in the small intestine and then widely distributed to target tissues, microarray analyses were performed to compare the expression levels of transport-related genes in the duodenum between C57BL/6J mice and 129/Sv or DBA/2 mice.

Gene expression analysis using DNA microarray in HK-2 human proximal tubular cells treated with cadmium.

We examined the alteration of gene expression in HK-2 human proximal tubular cells exposed to cadmium (Cd) using DNA microarray analysis. Cd increased the expression of 30 genes, including 7 genes coding for heat shock proteins, more than 2.0-fold and decreased the expression of 21 genes, including transcription-related genes, such as AP2B1, HOXA7, HOXA9 and TCEB2, less than 0.

Inorganic arsenic induces apoptosis through downregulation of Ube2d genes and p53 accumulation in rat proximal tubular cells.

Ube2d ubiquitin-conjugating enzymes promote p53 ubiquitination and proteasomal degradation. We previously showed that cadmium induced p53-dependent apoptosis through the suppression of expression of Ube2d family genes (Ube2d1, Ube2d2, Ube2d3 and Ube2d4) in normal rat proximal tubular cells. Here we examined the effects of inorganic arsenic and inorganic mercury, which induce apoptosis in proximal tubular cells, on cellular protein level of p53 and gene expression of Ube2d family.

DNA microarray expression analysis of mouse kidney following cadmium exposure for 12 months.

Cadmium (Cd) is a toxic heavy metal and chronic exposure causes kidney injury. This study used DNA microarray analysis to examine gene expression in the kidney of mice chronically exposed to Cd. Female C57BL/6J mice were fed a 300 ppm Cd-containing diet or a control diet for 12 months.

Chromatographic behavior of selenoproteins in rat serum detected by inductively coupled plasma mass spectrometry.

Two major selenoproteins are present in mammalian serum: extracellular glutathione peroxidase (eGPx) and selenoprotein P (Sel P). The chromatographic behaviors of the two serum selenoproteins were compared in four rodent species, and the selenoproteins in rat serum were identified by measuring enzyme activity and Western blotting. The selenoproteins in rat serum showed a specific chromatographic behavior.

Speciation and identification of tellurium-containing metabolites in garlic, Allium sativum.

Tellurium (Te) is a widely used metalloid in industry because of its unique chemical and physical properties. However, information about the biological and toxicological activities of Te in plants and animals is limited. Although Te is expected to be metabolized in organisms via the same pathway as sulfur and selenium (Se), no precise metabolic pathways are known in organisms, particularly in plants.

DNA microarray analysis of hepatic gene expression in mice exposed to cadmium for 30 days.

Although cadmium causes hepatotoxicity, its molecular mechanism is unclear. In the present study, transcriptional responses in the liver of C57BL/6J mice given 50 ppm cadmium as a drinking water for 30 days were evaluated with DNA microarray. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were not elevated following the administration of cadmium.

Cadmium renal toxicity via apoptotic pathways.

Cadmium is a nonessential heavy metal and ubiquitous potential environmental pollutant. Although the kidney proximal tubule is an important target for cadmium, the underlying cellular mechanisms of cadmium-induced renal toxicity remain elusive. Numerous studies have demonstrated that cadmium induces apoptotic cell death in various cell types via several apoptotic pathways, including mitochondria-mediated apoptotic cell death.

[Cadmium induces p53-dependent apoptosis through the inhibition of Ube2d family gene expression].

Cadmium (Cd), a harmful metal, exerts severe toxic effects on various tissues such as those in the kidney, liver, lung, and bone. In particular, renal toxicity with damage to proximal tubule cells is caused by chronic exposure to Cd. However, the molecular mechanism underlying chronic Cd renal toxicity remains to be understood.