Nicotine upregulates the expression of P2Y12 on vascular cells and megakaryoblasts.

Background: P2Y12 is the major platelet receptor that mediates ADP-induced aggregation. P2Y12 is also expressed by vascular cells. The factors that regulate P2Y12 expression have not been determined.

Mercuric chloride inhibits the in vitro uptake of glutamate in GLAST- and GLT-1-transfected mutant CHO-K1 cells.

Glutamate is removed mainly by astrocytes from the extracellular fluid via high-affinity astroglial Na+ -dependent excitatory amino acid transporters, glutamate/aspartate transporter (GLAST), and glutamate transporter-1 (GLT-1). Mercuric chloride (HgCl2) is a highly toxic compound that inhibits glutamate uptake in astrocytes, resulting in excessive extracellular glutamate accumulation, leading to excitotoxicity and neuronal cell death. The mechanisms associated with the inhibitory effects of HgCl2 on glutamate uptake are unknown.

In vitro uptake of glutamate in GLAST- and GLT-1-transfected mutant CHO-K1 cells is inhibited by the ethylmercury-containing preservative thimerosal.

Thimerosal, also known as thimersal, Merthrolate, or sodiumethyl-mercurithiosalicylate, is an organic mercurial compound that is used in a variety of commercial as well as biomedical applications. As a preservative, it is used in a number of vaccines and pharmaceutical products. Its active ingredient is ethylmercury.

Modulatory effect of glutathione status and antioxidants on methylmercury-induced free radical formation in primary cultures of cerebral astrocytes.

Excessive free radical formation has been implicated as one of the causative factors in neurotoxic damage associated with variety of metals, including methylmercury (MeHg). Although the mechanism(s) associated with MeHg-dependent neurotoxicity remains far from clear, overwhelming data give credence to a mediatory role for astrocytes, a major cell type that preferentially accumulates MeHg. To extend our recent findings of MeHg-induced increase in ROS formation (G.

Free radical formation in cerebral cortical astrocytes in culture induced by methylmercury.

Oxidative stress has been implicated in neurotoxic damage associated with various metals, including methylmercury (MeHg). Although the mechanism(s) of MeHg-induced neurotoxicity remains unclear, evidence supports a mediatory role for astrocytes, a cell type that preferentially accumulates MeHg. Using scanning confocal microscopy (LSCM), the present study was undertaken to examine the role of astrocytes as the site of reactive oxygen species (ROS).

Methylmercury stimulates arachidonic acid release and cytosolic phospholipase A2 expression in primary neuronal cultures.

Cytosolic phospholipase A2 (cPLA2) plays an important role in the stimulus-dependent hydrolysis of sn-2 ester bond from membrane phospholipids, releasing arachidonic acid (AA), which along with its metabolites is involved in a number of regulatory functions. The present study examined the effect of methylmercury (MeHg; 0, 2.5, 5.

Astrocyte-mediated methylmercury neurotoxicity.

Methylmercury (MeHg) is a potent neurotoxicant. Any source of environmental mercury represents a potential risk for human MeHg poisoning, because the methylation of inorganic mercury to MeHg in waterways results ultimately in its accumulation in the sea food chain, which represents the most prevalent source for human consumption. A small amount of MeHg accumulates in the central nervous system (CNS), particularly in astrocytes.

Methylmercury-induced reactive oxygen species formation in neonatal cerebral astrocytic cultures is attenuated by antioxidants.

Excessive generation of reactive oxygen species (ROS) has been suggested as a causal factor in various neurodegenerative disorders, such as Parkinson's disease and Alzheimer's disease [Brain Res. 830 (1999) 10-15; Biochem. J.

The consequences of methylmercury exposure on interactive functions between astrocytes and neurons.

Methylmercury (MeHg) is a highly neurotoxic, environmentally ubiquitous chemical that exerts its toxic effects by largely unknown mechanisms. Maintenance of optimal intracellular concentrations of glutathione (GSH) is vital for cellular defenses against damage from free radicals. Since astrocytes play an essential role in providing GSH precursors to neurons, studies were directed at the effect of MeHg on cystine transport in both cell types.

Methylmercury enhances arachidonic acid release and cytosolic phospholipase A2 expression in primary cultures of neonatal astrocytes.

Cytosolic phospholipase A(2) (cPLA(2)) stimulates the hydrolysis of sn-2 ester bond in membrane phospholipids releasing arachidonic acid (AA) and lysophospholipids. The present study examined the effect of methylmercury (MeHg) on cPLA(2) activation and AA release in primary cultures of neonatal rat cerebral astrocytes. Astrocytes were preloaded overnight at 37 degrees C with 3H-AA to metabolically label phospholipids.

The uptake of manganese in brain endothelial cultures.

The present study focused on central nervous system (CNS) transport kinetics of manganese phosphate and manganese sulfate; these findings were correlated with the transport kinetics of manganese chloride (MnCl2), a model Mn compound that has been previously studied. A series of studies was performed to address the transport of Mn salts in confluent cultured endothelial cells. The initial rate of uptake (5 min) of Mn salts (chloride, sulfate, and phosphate) in rat brain endothelial (RBE4) cell cultures is salt-dependent, with the highest rates of uptake for Mn chloride and Mn sulfate (as reflected by the greatest displacement of 54Mn compared with control).