Activation and inactivation of taurine efflux in hyposmotic and isosmotic swelling in cortical astrocytes: Role of ionic strength and cell volume decrease

Abstract

A decrease in intracellular ionic strength appears involved in the activation of swelling-elicited 3H-taurine efflux in cortical cultured astrocytes. Hyposmotic (50%) or isosmotic urea-induced swelling leading to a decrease of intracellular ionic strength, activated 3H-taurine efflux from a rate constant of about 0.008 min(-1) to 0.33 min(-1) (hyposmotic) and 0.59 min(-1) (urea). This efflux rate was markedly lower (maximal 0.03 min(-1)) in isosmotic swelling caused by K+ accumulation, where there is no decrease in ionic strength, or in cold (10 degrees C) hyposmotic medium (maximal 0.18 min(-1)), where swelling is reduced and consequently intracellular ionic strength is less affected. Also, astrocytes pretreated with hyperosmotic medium, which recover cell volume by ion accumulation, did not release 3H-taurine when they swelled by switching to isosmotic medium, but when volume was recovered by accumulation of urea, taurine release was restored. These results point to a key role of ionic strength in the activation of osmosensitive 3H-taurine efflux. In contrast, its inactivation was independent of the change in ionic strength but appears related to the reduction in cell volume after swelling, since despite the extent or direction of the change in ionic strength, the 3H-taurine efflux did not inactivate in isosmotic KCl-elicited swelling when cell volume did not recover nor in hyposmotic swelling when RVD was impaired by replacing NaCl in the medium by permeant osmolytes.

Channels and Volume Changes in the Life and Death of the Cell

“…As clearly underlined in Shennan (2008) and Stutzin et al (1999), if taurine and Cl -hypotonic fluxes were occurring via an identical pathway, such large differences in the time course should not be observed. Though similar to VRAC-mediated currents, isotonic taurine efflux is evoked by a decrease in ionic strength (Cardin et al, 1999;Guizouarn and Motais, 1999). The recent discovery of the LRRC8 family of proteins forming volume-sensitive heteromeric channels with different permeability offers a real possibility to establish the molecular identity of the organic osmolyte efflux pathway(s).…”

Hepatoprotective Effect of Taurine Against Oxidative Stress Due to Methotrexate in Rat

“…Activated neutrophils also release proteolytic enzymes that have the capacity to alter alveolar interstitial components. It was proposed by Gordon et al (1986) and Cardin et al (1999) that the protective activity of taurine may reside in its ability to become chlorinated in the presence of HOCL, thereby preventing the direct attack of this oxidant on cell membranes (Rock et al, 1996). Lee et al (1992) postulated that the protective action of taurine on oxidant-induced damages of tissue components including degradation of hyaluronic acid may be attributed to both its scavenging action on hypochloriate (HOCl) and chloramine and the complex formation of taurine with HOCl or NH2Cl without scavenging action on oxygen free radicals.…”

Thrombin potentiates d‐aspartate efflux from cultured astrocytes under conditions of K+ homeostasis disruption

“…This is a predictable result since the typical regulatory volume decrease observed under hyposmotic conditions is accomplished to a large extent, by K + and Cl − extrusion (Wehner 1998; Stutzin and Hoffmann 2006) which cannot occur in high extracellular K + concentrations. The pool of organic osmolytes, including glutamate, taurine and myo‐inositol (Rutledge and Kimelberg 1996; Cardin et al. 1999; Isaacks et al.…”