Extensive studies have indicated that the apoptosis pathway appears to be associated with intracellular reactive oxygen species (ROS) production in cadmium-induced nephrotoxicity, however, the precise cellular mechanism remains unclear. The purpose of this study was to determine the relationships between the activation of phosphorylated c-jun N-terminal kinase (JNK) and cadmium-induced apoptosis, and assess the possible cytoprotective mechanism of selenium. Our study clearly revealed cadmium treatment caused apoptosis in LLC-PK1 cells, which was partially suppressed by pretreatment with selenium, an antioxidant nutrient. Further studies found the phosphorylation of JNK kinase increased with exposure to cadmium for 3 h, even remained elevated at 9 h in the time course study, and the activation of phosphorylated JNK was detected in a dose-dependent manner. In addition, a concomitant time-dependent increase in caspase-3 activities was observed by cadmium treatment. During the process, selenium played the same role as N-acetyl-L-cysteine (NAC), a free radical scavenger. Pretreatment of cells with selenium partially suppressed of the phosphorylation of JNK, coupled with caspase-3 activation involved in cadmium-induced apoptosis. In ...Continue Reading
Interactions of selenium and cadmium with metallothionein-like and other cytosolic proteins of rat kidney and liver
JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain
The role of c-Jun N-terminal kinase (JNK) in apoptosis induced by ultraviolet C and gamma radiation. Duration of JNK activation may determine cell death and proliferation.
The cellular response to oxidative stress: influences of mitogen-activated protein kinase signalling pathways on cell survival
Characterization of cadmium-induced apoptosis in rat lung epithelial cells: evidence for the participation of oxidant stress
Up-regulation of multidrug resistance P-glycoprotein via nuclear factor-kappaB activation protects kidney proximal tubule cells from cadmium- and reactive oxygen species-induced apoptosis
Roles of JNK, p38 and ERK mitogen-activated protein kinases in the growth inhibition and apoptosis induced by cadmium
Cadmium induces apoptosis and genotoxicity in rainbow trout hepatocytes through generation of reactive oxygene species
Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple
Cadmium-dependent generation of reactive oxygen species and mitochondrial DNA breaks in photosynthetic and non-photosynthetic strains of Euglena gracilis
Calcium-mediated activation of c-Jun NH2-terminal kinase (JNK) and apoptosis in response to cadmium in murine macrophages
Cd(2+)-induced cytochrome c release in apoptotic proximal tubule cells: role of mitochondrial permeability transition pore and Ca(2+) uniporter
Role of mitogen activated protein kinases and protein kinase C in cadmium-induced apoptosis of primary epithelial lung cells
A rapid and transient ROS generation by cadmium triggers apoptosis via caspase-dependent pathway in HepG2 cells and this is inhibited through N-acetylcysteine-mediated catalase upregulation
Cadmium-induced apoptosis in rat kidney epithelial cells involves decrease in nuclear factor-kappa B activity
Cadmium induces reactive oxygen species generation and lipid peroxidation in cortical neurons in culture
Cadmium-induced apoptosis in murine macrophages is antagonized by antioxidants and caspase inhibitors
Synergistic effects of 5-fluorouracil and gambogenic acid on A549 cells: activation of cell death caused by apoptotic and necroptotic mechanisms via the ROS-mitochondria pathway
Cadmium-induced injury and the ameliorative effects of selenium on chicken splenic lymphocytes: mechanisms of oxidative stress and apoptosis
Induction of autophagy in porcine kidney cells by quantum dots: a common cellular response to nanomaterials?
Probing and preventing quantum dot-induced cytotoxicity with multimodal alpha-lipoic acid in multiple dimensions of the peripheral nervous system
Biological responses related to agonistic, antagonistic and synergistic interactions of chemical species
B1, a novel naphthalimide-based DNA intercalator, induces cell cycle arrest and apoptosis in HeLa cells via p53 activation.
An in vitro examination of selenium-cadmium antagonism using primary cultures of rainbow trout (Oncorhynchus mykiss) hepatocytes
The SMAD2/3 pathway is involved in hepaCAM-induced apoptosis by inhibiting the nuclear translocation of SMAD2/3 in bladder cancer cells
Activation of Nrf2 by cadmium and its role in protection against cadmium-induced apoptosis in rat kidney cells
The role of MAPK in the biphasic dose-response phenomenon induced by cadmium and mercury in HEK293 cells
The protection of selenium on ROS mediated-apoptosis by mitochondria dysfunction in cadmium-induced LLC-PK(1) cells
HDAC inhibitor DWP0016 activates p53 transcription and acetylation to inhibit cell growth in U251 glioblastoma cells
Low-Dose Cadmium Causes Metabolic and Genetic Dysregulation Associated With Fatty Liver Disease in Mice
Pseudolaric acid B induces apoptosis via proteasome-mediated Bcl-2 degradation in hormone-refractory prostate cancer DU145 cells
EGCG inhibits Cd(2+)-induced apoptosis through scavenging ROS rather than chelating Cd(2+) in HL-7702 cells
Activation of liver X receptors inhibits cadmium-induced apoptosis of human renal proximal tubular cells
The protection of selenium on cadmium-induced inhibition of spermatogenesis via activating testosterone synthesis in mice
The protective effects of selenium on cadmium-induced oxidative stress and apoptosis via mitochondria pathway in mice kidney
The role of Sep (O-phosphoserine) tRNA: Sec (selenocysteine) synthase (SEPSECS) in proliferation, apoptosis and hormone secretion of trophoblast cells
The synthesis of sulforaphane analogues and their protection effect against cisplatin induced cytotoxicity in kidney cells.
2-[5-Selenocyanato-pentyl]-6-amino-benzo[de]isoquinoline-1,3-dione inhibits angiogenesis, induces p53 dependent mitochondrial apoptosis and enhances therapeutic efficacy of cyclophosphamide
Bone marrow microenvironment confers imatinib resistance to chronic myelogenous leukemia and oroxylin A reverses the resistance by suppressing Stat3 pathway
Global gene expression analysis of cellular death mechanisms induced by mesoporous silica nanoparticle-based drug delivery system
Protective effect of N-acetylcysteine on experimental chronic cadmium nephrotoxicity in immature female rats
DBA-induced caspase-3-dependent apoptosis occurs through mitochondrial translocation of cyt-c in the rat hippocampus
A Valid Bisphosphonate Modified Calcium Phosphate-Based Gene Delivery System: Increased Stability and Enhanced Transfection Efficiency In Vitro and In Vivo
Metabolic impairments, metal traffic, and dyshomeostasis caused by the antagonistic interaction of cadmium and selenium using organic and inorganic mass spectrometry
Exopolysaccharides produced by Lactobacillus strains suppress HT-29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis
Curcumin increases the sensitivity of K562/DOX cells to doxorubicin by targeting S100 calcium-binding protein A8 and P-glycoprotein
Overexpression of oxidored-nitro domain containing protein 1 induces growth inhibition and apoptosis in human prostate cancer PC3 cells
Hepatotoxic Effect of Oral Zinc Oxide Nanoparticles and the Ameliorating Role of Selenium in Rats: A histological, immunohistochemical and molecular study.
Interaction of prenatal bisphenols, maternal nutrients, and toxic metal exposures on neurodevelopment of 2-year-olds in the APrON cohort.
Trace elements in children with autism spectrum disorder: A meta-analysis based on case-control studies.
Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.
Bioinformatics in Biomedicine
Bioinformatics in biomedicine incorporates computer science, biology, chemistry, medicine, mathematics and statistics. Discover the latest research on bioinformatics in biomedicine here.
Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis