Elevations of Intracellular Ca 2+ as a Probable Contributor to Decreased Viability in Cerebellar Granule Cells Following Acute Exposure to Methylmercury

Elevations of Intracellular Ca 2+ as a Probable Contributor to Decreased Viability in Cerebellar... In these experiments we examined whether the elevations in intracellular Ca 2+ concentration ((Ca 2+ ) i ) induced by methylmercury (MeHg) (described in our previous study) might contribute to cerebellar granule cell mortality following exposure to MeHg in vitro. Cells were exposed to 0.5 μM MeHg for 45 min or 1 μM MeHg for 38 min, conditions previously shown to induce elevations in (Ca 2+ ) i in these cells. Control cells were exposed to buffer alone for 60 min. Viability was assessed using the Live/Dead viability/cytotoxicity kit. At 30 min post-MeHg exposure, there was no immediate increase in cell mortality; however, by 3.5 h after the onset of MeHg exposure, cell viability decreased to 74 and 54% of control values for 0.5 and 1.0 μM MeHg, respectively. At 24.5 h after MeHg exposure, cell viability declined to approximately 27%. Losses in cell viability at 3.5 h were prevented by pretreating the granule cells for 65 min with the Ca 2+ chelator 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′ -tetraacetic acid tetrakis(acetoxymethyl)ester (BAPTA; 10 μM), then exposing the cells to MeHg in the continued presence of BAPTA; however, at 24.5 h, BAPTA no longer prevented MeHg-induced cell death. Exposure to the Ca 2+ channel blockers ω-conotoxin MVIIC (1 μM) or nifedipine (1 μM), previously shown to delay elevations in (Ca 2+ ) i with MeHg exposure in vitro, protected granule cells from MeHg-induced mortality at 3.5 h postexposure. These data suggest that at early time points, MeHg-induced increases in (Ca 2+ ) i may contribute to granule cell mortality; however, the role of Ca 2+ at later time points is unclear. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Toxicology and Applied Pharmacology Elsevier

Elevations of Intracellular Ca 2+ as a Probable Contributor to Decreased Viability in Cerebellar Granule Cells Following Acute Exposure to Methylmercury

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Publisher
Elsevier
Copyright
Copyright © 1998 Academic Press
ISSN
0041-008x
D.O.I.
10.1006/taap.1998.8383
Publisher site
See Article on Publisher Site

Abstract

In these experiments we examined whether the elevations in intracellular Ca 2+ concentration ((Ca 2+ ) i ) induced by methylmercury (MeHg) (described in our previous study) might contribute to cerebellar granule cell mortality following exposure to MeHg in vitro. Cells were exposed to 0.5 μM MeHg for 45 min or 1 μM MeHg for 38 min, conditions previously shown to induce elevations in (Ca 2+ ) i in these cells. Control cells were exposed to buffer alone for 60 min. Viability was assessed using the Live/Dead viability/cytotoxicity kit. At 30 min post-MeHg exposure, there was no immediate increase in cell mortality; however, by 3.5 h after the onset of MeHg exposure, cell viability decreased to 74 and 54% of control values for 0.5 and 1.0 μM MeHg, respectively. At 24.5 h after MeHg exposure, cell viability declined to approximately 27%. Losses in cell viability at 3.5 h were prevented by pretreating the granule cells for 65 min with the Ca 2+ chelator 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′ -tetraacetic acid tetrakis(acetoxymethyl)ester (BAPTA; 10 μM), then exposing the cells to MeHg in the continued presence of BAPTA; however, at 24.5 h, BAPTA no longer prevented MeHg-induced cell death. Exposure to the Ca 2+ channel blockers ω-conotoxin MVIIC (1 μM) or nifedipine (1 μM), previously shown to delay elevations in (Ca 2+ ) i with MeHg exposure in vitro, protected granule cells from MeHg-induced mortality at 3.5 h postexposure. These data suggest that at early time points, MeHg-induced increases in (Ca 2+ ) i may contribute to granule cell mortality; however, the role of Ca 2+ at later time points is unclear.

Journal

Toxicology and Applied PharmacologyElsevier

Published: May 1, 1998

References

  • Nifedipine and tetrodotoxin delay the onset of methylmercury-induced increases in (Ca 2+ ) i in NG108-15 cells
    Hare, M.F.; Atchison, W.D.
  • Susceptibility of lipids to mercurials
    Nakada, S.; Imura, N.
  • Decrease in calcium currents induced by aminoglycoside antibiotics in frog motor nerve endings
    Redman, R.S.; Silinsky, E.M.
  • Methyl mercury inhibition of synaptosome and brain slice protein synthesis: In vivo and in vitro studies
    Verity, M.A.; Brown, W.J.; Cheung, M.; Czer, G.
  • Biochemical changes in the brain in rats poisoned with an alkylmercury compound, with special reference to the inhibition of protein synthesis in brain cortex slices
    Yoshino, Y.; Mozai, T.; Nakao, K.

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