The protective effects of selenium on cadmium-induced oxidative stress and apoptosis via mitochondria pathway in mice kidney

Wang, Yang; Wu, Yuchen; Luo, K.X.; Liu, Yuxin; Zhou, Ming; Yan, Shijuan; Shi, Hui; Cai, Yuanqing

doi:10.1016/j.fct.2013.04.013

Cited by 142 publications

(72 citation statements)

References 31 publications

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“…Increased Bax/Bcl-2 ratio triggers Bax translocation to mitochondria to form a VDAC channel for promoting cytochrome c release and caspase 3 activation [33], [34]. We confirm that activated Bax/Bcl-2 ratio, caspase 3, and PARP signaling contributes to acetic acid-induced duodenal ulceration.…”

Section: Discussionsupporting

confidence: 66%

“…Ingestion of DSW600, DSW1200, or selenium upregulates Trxnrd1 as well as Bcl-2 expression and downregulates Bax in duodenal cells. Pretreatment with selenium partially blocked cadmium-induced ROS production, mitochondrial membrane potential collapse, cytochrome c release, and caspase activation, and altered Bcl-2 and Bax levels [34]. Selenium also enhanced glutathione peroxidase-1 and Trxnrd1 expression, providing vascular endothelial protection [35].…”

Section: Discussionmentioning

confidence: 98%

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Deep-Sea Water Containing Selenium Provides Intestinal Protection against Duodenal Ulcers through the Upregulation of Bcl-2 and Thioredoxin Reductase 1

Yang

Yao

Lin³

et al. 2014

PLoS ONE

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Deep-sea water (DSW), which is rich in micronutrients and minerals and with antioxidant and anti-inflammatory qualities, may be developed as marine drugs to provide intestinal protection against duodenal ulcers. We determined several characteristics in the modified DSW. We explored duodenal pressure, oxygenation, microvascular blood flow, and changes in pH and oxidative redox potential (ORP) values within the stomach and duodenum in response to tap water (TW, hardness: 2.48 ppm), DSW600 (hardness: 600 ppm), and DSW1200 (hardness: 1200 ppm) in Wistar rats and analyzed oxidative stress and apoptosis gene expressions by cDNA and RNA microarrays in the duodenal epithelium. We compared the effects of drinking DSW, MgCl2, and selenium water on duodenal ulcers using pathologic scoring, immunohistochemical analysis, and Western blotting. Our results showed DSW has a higher pH value, lower ORP value, higher scavenging H2O2 and HOCl activity, higher Mg2+ concentrations, and micronutrients selenium compared with TW samples. Water infusion significantly increased intestinal pressure, O2 levels, and microvascular blood flow in DSW and TW groups. Microarray showed DSW600, DSW1200, selenium water upregulated antioxidant and anti-apoptotic genes and downregulated pro-apoptotic gene expression compared with the TW group. Drinking DSW600, DSW1200, and selenium water but not Mg2+ water significantly enhanced Bcl-2 and thioredoxin reductase 1 expression. Bax/Bcl-2/caspase 3/poly-(ADP-ribose)-polymerase signaling was activated during the pathogenesis of duodenal ulceration. DSW drinking reduced ulcer area as well as apoptotic signaling in acetic acid-induced duodenal ulcers. DSW, which contains selenium, provides intestinal protection against duodenal ulcers through the upregulation of Bcl-2 and thioredoxin reductase 1.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 98%

Deep-Sea Water Containing Selenium Provides Intestinal Protection against Duodenal Ulcers through the Upregulation of Bcl-2 and Thioredoxin Reductase 1

Yang

Yao

Lin³

et al. 2014

PLoS ONE

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“…Bcl-2 family can affect and regulate the mitochondrial permeability and play critical roles in modulating mitochondria-mediated apoptosis [44,45]. Hence, the balance between pro-apoptotic proteins (Bax, Bad, Bid, and Bim) and anti-apoptotic proteins (Bcl-2, Bcl-xL, Mcl-1, and Bcl-w) ultimately decides the fate of the cells [46]. Our results revealed that high glucoseinduced apoptosis involved the unbalance of Bcl-2 family protein expression, whereas pretreatment with DSePA significantly inhibited the downregulation of Bcl-xL and Bcl-2.…”

Section: Discussionmentioning

confidence: 99%

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

Wang

et al. 2015

Mol Neurobiol

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Hyperglycemia as the major hallmark of diabetic neuropathy severely limited its therapeutic efficiency. Evidences have revealed that selenium (Se) as an essential trace element could effectively reduce the risk of neurological diseases. In the present study, 3,3'-diselenodipropionic acid (DSePA), a derivative of selenocystine, was employed to investigate its protective effect against high glucose-induced neurotoxicity in PC12 cells and evaluate the underlying mechanism. The results suggested that high glucose showed significant cytotoxicity through launching mitochondria-mediated apoptosis in PC12 cells, accompanied by poly (ADP-ribose) polymerase (PARP) cleavage, caspase activation, and mitochondrial dysfunction. Moreover, high glucose also triggered DNA damage and dysregulation of MAPKs and AKT pathways through reactive oxygen species (ROS) overproduction. p53 RNA interference partially suppressed high glucose-induced cytotoxicity and apoptosis, indicating the role of p53 in high glucose-induced signal. However, DSePA pretreatment effectively attenuated high glucose-induced cytotoxicity, inhibited the mitochondrial dysfunction through regulation of Bcl-2 family, and ultimately reversed high glucose-induced apoptotic cell death in PC12 cells. Attenuation of caspase activation, PARP cleavage, DNA damage, and ROS accumulation all confirmed its protective effects. Moreover, DSePA markedly alleviated the dysregulation of AKT and MAPKs pathways induced by high glucose. Our findings revealed that the strategy of using DSePA to antagonize high glucose-induced neurotoxicity may be a highly effective strategy in combating high glucose-mediated neurological diseases.

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“…It has been documented that this pathway of apoptosis includes the disturbance in the expression of Bcl-2 family members, loss of mitochondrial transmembrane potential (MMP), release of cytochrome c from the mitochondria into the cytoplasm, activation of caspase-3 and ultimately trigger apoptosis17, 18 ) . Bax and Bcl-2 are representative members of the Bcl-2 family.…”

Section: Introductionmentioning

confidence: 99%

2,5-hexanedione induced apoptosis in mesenchymal stem cells from rat bone marrow via mitochondria-dependent caspase-3 pathway

et al. 2015

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2,5-hexanedione (HD) induces apoptosis of nerve cells. However,the mechanism of HD-induced apoptosis remains unknown. Mesenchymal stem cells (MSCs) are multipotential stem cells with the ability to differentiate into various cell types. This study is designed to investigate the apoptosis induced by HD in rat bone marrow MSCs (BMSCs) and the related underlying mechanisms. The fifth generation of MSCs was treated with 0, 10, 20 and 40 mM HD respectively. The viability of BMSCs was observed by MTT. Apoptosis were estimated by Hoechst 33342 staining and TUNEL assay. The disruption of mitochondrial transmembrane potential (MMP) was examined by JC-1 staining. Moreover, the expression of Bax and Bcl-2, cytochrome c release, and caspase-3 activity were determined by real-time RT-PCR, Western blot and Spectrophotometry. Our results showed that HD induced apoptosis in MSCs in a dose dependent manner. Moreover, HD downregulated the Bcl-2 expression,upregulated the Bax expression and the Bax/Bcl-2 ratio, promoted the disruption of MMP, induced the release of cytochrome c from mitochondria to cytosol, and increased the activity of caspase-3 in MSCs. These results indicate that HD induces apoptosis in MSCs and the activated mitochondria-dependent caspase-3 pathway may be involved in the HD-induced apoptosis.

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The protective effects of selenium on cadmium-induced oxidative stress and apoptosis via mitochondria pathway in mice kidney

Cited by 142 publications

References 31 publications

Deep-Sea Water Containing Selenium Provides Intestinal Protection against Duodenal Ulcers through the Upregulation of Bcl-2 and Thioredoxin Reductase 1

Deep-Sea Water Containing Selenium Provides Intestinal Protection against Duodenal Ulcers through the Upregulation of Bcl-2 and Thioredoxin Reductase 1

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

2,5-hexanedione induced apoptosis in mesenchymal stem cells from rat bone marrow via mitochondria-dependent caspase-3 pathway

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