Intracellular calcium and neurotoxic events

Bondy, Stephen C.

doi:10.1016/0892-0362(89)90032-9

Cited by 21 publications

(8 citation statements)

References 51 publications

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“…Comparison of the effects of congeners within chemical classes has in several cases revealed a relation between the ability of a compound to effect synaptosomal damage and its relative neurotoxicity. This has been reported for isomers of hexachlorocyclohexane, various alkyl lead compounds, and for the organochlorine insecticides mirex and chlordecone (Bondy, 1989).…”

Section: Introductionmentioning

confidence: 66%

“…Synaptosomes are vulnerable to damage due to a variety of adverse conditions. These include exposure to oxidative conditions (Debler et al, 1986;Braughler, 1985;Bondy et a]., 1989), heavy metals (Atchison et al, 1986;Komulainen and Bondy, 1987a), organic solvents (Michaelis and Myers, 1982;Harris and Bruno, 1985;Korpela and Tahti, 1988;Daniel1 et al, 1988), and insecticides (Yamaguchi et al, 1979;Komulainen and Bondy, 1987b;Bondy and Halsall, 1988a). Comparison of the effects of congeners within chemical classes has in several cases revealed a relation between the ability of a compound to effect synaptosomal damage and its relative neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

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Prevention of chemically induced synaptosomal changes

Bondy

McKee

1990

J of Neuroscience Research

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The ability of altered environmental conditions to modulate some properties of synaptosomes has been studied. Incubation conditions used included the presence of methyl mercury or an organochlorine insecticide: chlordecone. Other adverse chemical conditions during incubation were the absence of calcium salts from the incubation medium or the addition of agents bringing about enhanced oxidative conditions. Synaptosomal parameters studied were the cytosolic level of free, ionic calcium, [Ca2+]i, the extent of depolarization-induced uptake of radioactive calcium, and the permeability of the limiting membrane. In addition, peroxidative activity was estimated by quantitation of thiobarbituric acid-reactive material. All these facets of synaptosomal function were responsive to the presence of these potentially deleterious changes in the incubation medium. While the response of [Ca2+]i was potentially in either direction, all adverse conditions increased synaptosomal permeability as evaluated by leakage of fura-2 into the extracellular compartment. Pretreatment with ganglioside GM1 in some situations or alpha-tocopherol in others could either wholly or partially prevent the onset of such altered synaptosomal characteristics.

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Section: Introductionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Prevention of chemically induced synaptosomal changes

Bondy

McKee

1990

J of Neuroscience Research

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“…Excitotoxic neuronal death resulting from overstimulation of glutamate receptors is mediated by calcium influx (Verity, 1992) through both NMDA and non-NMDA-type glutamate receptors (Bondy, 1989;Siesjo, 1989;Brorson et al, 1992). The resulting increase in intracellular calcium content is postulated to activate protein kinases, lipases, phosphatases, and possibly endonucleases (Siesjo, 1992;Verity, 1992), all of which may play a role in delayed neuronal death.…”

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confidence: 99%

Aurintricarboxylic Acid Protects Hippocampal Neurons from Glutamate Excitotoxicity In Vitro

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Dubinsky

1993

Journal of Neurochemistry

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Aurintricarboxylic acid (ATA), an endonuclease inhibitor, has been shown to protect several cell types from an apoptotic form of cell death. We tested ATA for protective effects against glutamate excitotoxicity in 2-week-old cultured hippocampal neurons. Cell viability was determined 24 h after glutamate exposure either by trypan blue exclusion or by measurement of lactate dehydrogenase release. When ATA was added during exposure to glutamate, there was a dramatic increase in the number of viable neurons compared with cultures that did not receive ATA. If ATA was added after glutamate exposure, the rate of survival approached 100%. Several cellular processes may be the targets for ATA action. If the mechanisms of ATA protection are similar for excitotoxicity and apoptosis, then these distinct forms of cell death may share a common intracellular pathway.

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“…(Nicotera et al, 1989). Direct chemical plasma nrembrane injury (Bondy, 1989) may perturb [Ca 2+ ]ĥ omeostasis, e.g., by facilitating Ca 2+ influx. Generated from EBDC metabolites (Edwards et al, 1991), reactive forms of sulfur may bind to proteins involved in Ca 2+ regulation.…”

Section: Resultsmentioning

confidence: 99%

Elevation of intracellular free calcium levels in sperm in response to long-term feeding of fungicides to mice

Shi

Chen

Chou

et al. 1992

J. of Env. Sc. & Hlth., Part B

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To assess the impact of long-term feeding of fungicides on sperm quality, mice were fed a daily diet containing a mixture of maneb and zineb, at concentrations of 30, 300, and 3000 ppm, respectively. Employing epididymal sperm suspended in a medium permitting in vitro capacitation, the intracellular free Ca2+ concentration, [Ca2+]i, was determined with a fluorescent Ca2+ indicator, Fura-2. Regardless of the fungicide dosages applied, [Ca2+]i was about 50 percent higher in treated animals relative to a value of 123 nM [Ca2+]i in the control group. Fungicide-treated mice were mated to mature, non-treated females; as in the control, the litter sizes were the same. In conclusion, the observed elevation in [Ca2+]i seems to reflect cellular adaptation responses to toxic stress at moderate fungicide doses.

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Intracellular calcium and neurotoxic events

Cited by 21 publications

References 51 publications

Prevention of chemically induced synaptosomal changes

Prevention of chemically induced synaptosomal changes

Aurintricarboxylic Acid Protects Hippocampal Neurons from Glutamate Excitotoxicity In Vitro

Elevation of intracellular free calcium levels in sperm in response to long-term feeding of fungicides to mice

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