Key result
Intracellular calcium chelators such as QUIN 2/AM decreased oxidant-induced LDH release from 41% to as low as 4% in rabbit renal proximal tubule cells, likely by chelating iron.
Intracellular calcium chelators inhibit oxidant-induced cell death in rabbit renal proximal tubule cells, suggesting they act by chelating iron.
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Calcium chelators prevent oxidant-induced renal proximal tubule cell death in vitro; hypothesis-generating for cytoprotection but should not yet change practice.
The effect of intracellular calcium chelators on rabbit renal proximal tubule (RPT) cell death induced by t-butyl hydroperoxide (TBHP) and H2O2 was examined. Preincubation of RPT suspensions with 50 microM QUIN 2/AM completely prevented TBHP (0.5 mM) and H2O2 (2 mM) induced cell death [i.e., release of lactate dehydrogenase (LDH)]. QUIN 2/AM, BAPTA/AM, EGTA/AM, and FURA 2/AM, at 5 microM, decreased LDH release (at 6 hr) from 41% to 4%, 21%, 26%, and 33%, and decreased lipid peroxidation (at 1 hr) from 1.0 to 0.1, 0.4, 0.6, and 0.8 nmol MDA/mg protein, respectively, after TBHP exposure. Since oxidant-induced lipid peroxidation and cell death are iron-dependent in this model, these results suggest that the intracellular calcium chelators inhibit cell death by chelating iron.
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Rick G. Schnellmann (1991) studied Oxidant-induced cell death. Intracellular calcium chelators (QUIN 2/AM, BAPTA/AM, EGTA/AM, FURA 2/AM) vs. Oxidant exposure without chelators was evaluated on Cell death (LDH release). Intracellular calcium chelators such as QUIN 2/AM decreased oxidant-induced LDH release from 41% to as low as 4% in rabbit renal proximal tubule cells, likely by chelating iron.
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