<p style=/line-height:25px/>BAPTA is a specific chelator of Ca2+, suppresses intracellular reactive oxygen species (ROS) levels.<br>Target: Ca2+ chelator[1]<br>InVitro: Regarding ROS generation, a Ca2+ specific chelator, BAPTA, suppresses ROS generation of Sodium lauryl sulfate (SLS)-exposed HaCaT keratinocytes[1]. Depolarization does not increase the resting open probability of the mechanoelectrical transducer (MET) current of Tmc1Bth/Bth OHCs, whereas raising the intracellular concentration of the Ca2+ chelator BAPTA causes smaller increases in resting open probability in Bthmutant outer hair cells (OHCs) than in wild-type control cells. In the presence of 0.1 mM BAPTA, nonsaturating bundle displacements causes the MET current to adapt in both genotypes, exactly as seen when 1 mM EGTA is used in the intracellular solution. In the presence of 10 mM intracellular BAPTA, the time-dependent MET current decline is abolished and the resting Popen increased to near 50% of the maximal MET current in OHCs from both Tmc1+/+ and Tmc1Bth/Bth mice. The relation between the MET current and bundle displacement shows that increasing the intracellular BAPTA concentration from 0.1 to 10 mM significantly increased (p<0.0001) the resting Popen of the MET current in both Tmc1+/+ (0.1 mM, 8±1.6%, n=4; 10 mM, 39.6±2.7%, n=5) and Tmc1Bth/Bth (0.1 mM, 10.4±2.2%, n=3; 10 mM, 46.5±9.9%, n=6). No significant differences are seen between the two genotypes for both BAPTA concentrations. However, 3 and 5 mM BAPTA are less effective in shifting the MET current-bundle displacement curves in Tmc1Bth/Bth than in Tmc1+/+ OHCs. In Tmc1+/+, increasing the BAPTA concentration from 0.1 mM to either 3 or 5 mM produces a highly significant increase in Popen (post hoc test from one-way ANOVA, p<0.01 and p<0.001, respectively); in Tmc1Bth/Bth, the same comparison produced no or a much reduced increase in Popen (n.s. and p<0.05, respectively)[2].</p>
