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|Title:||Microsomal Ca<sup>2+</sup> flux modulation as an indicator of heavy metal toxicity|
Heavy metal toxicity
|Abstract:||Inositol 1,4,5-trisphosphatee (IP3), an intracellular messenger, releases Ca<sup>2+</sup> from microsomes. Ca<sup>2+</sup> plays a major role in regulating various cellular events like neural transmission and regulation of hormones and growth factors. Aluminum (Al), lead (Pb) and mercury (Hg) were reported to alter Ca<sup>2+</sup>-regulated events thereby causing neurotoxicity. Hence, an attempt was made characterize IP3 mediated Ca<sup>2+</sup> release from rat brain microsomes under the influence of Al, Pb and Hg. Different concentrations of metals were tested over a designated time scale and their effects on IP3 mediated Ca<sup>2+</sup> release from microsomes were monitored using Fura-2 technique. All the three metals inhibited IP3 mediated Ca<sup>2+</sup> release, Pb being more potent. The order of potency of these three metals was Pb>Hg>Al. Except for Al, both Hg and Pb independently released Ca<sup>2+</sup> from microsomes. Re-uptake of Ca<sup>2+</sup> into microsomes was inhibited by all the three metals, Pb being more potent. Microsomal Ca<sup>2+</sup>-ATPase activity was also inhibited by all the three metals. These results suggest that neurotoxicity exerted by Al, Pb and Hg may be due to the interference of these metals with IP3 mediated calcium release and also interfering with the microsomal Ca<sup>2+</sup> sequestration mechanism. Differential effects of heavy metal induced changes in Ca<sup>2+</sup> flux can be used as an index of relative toxicity.|
|ISSN:||0975-1009 (Online); 0019-5189 (Print)|
|Appears in Collections:||IJEB Vol.48(07) [July 2010]|
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