Contribution of plasma membrane and endoplasmic reticulum Ca2+-ATPases to the synaptosomal [Ca2+]i increase during oxidative stress

Pereira, Cláudia; Ferreira, Cristina; Carvalho, Caetana M.; Oliveira, Catarina R.

doi:10.1016/0006-8993(95)01554-x

Cited by 38 publications

(29 citation statements)

References 51 publications

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“…Interestingly, reactive oxygen species are known to inactivate SERCAs (Pereira et al 1996), which means ROS prevent the replenishing of internal stores and elicit a feedback, i.e hold/activate a continuous "call" of Ca 2+ from the external milieu in order to refill the "depleted stores" as shown in the present study (Figure 3.2A). This may further contribute to the long lasting activation of capacitative Ca 2+ influx.…”

Section: Ca 2+ Fluxes Affected By H 2 Omentioning

confidence: 52%

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Effects of H2O2 at rat myenteric neurones in culture

Pouokam

Rehn

Diener

2009

European Journal of Pharmacology

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Section: Ca 2+ Fluxes Affected By H 2 Omentioning

confidence: 52%

“…Thus it is an interesting implication that ROS are known to inactivate SERCA (Pereira et al 1996). Furthermore, free radicals such as OH deriving from hydrogen peroxide could participate as well in the age-related degenerative processes (Harman 1956).…”

Section: Diener and Gabato 1994)mentioning

confidence: 99%

Effects of H2O2 at rat myenteric neurones in culture

Pouokam

Rehn

Diener

2009

European Journal of Pharmacology

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“…The observed protective effects of divalent metals against low-cystine-type cell death and glutamate-induced cell death (Murphy et al, 1988) suggest that intracellular oxidants may be able to produce prolonged activation of voltage-sensitive Ca 2 + channels. The activity of voltage-dependent Ca 2 + channels and other Ca 2 + uptake systems, known to be sensitive to oxidation (Reeves et al, 1986;Roveri et al, 1992;Rohn et al, 1993;Pereira et al, 1996), does not seem to be compromised under our experimental conditions because the uptake of calcium was not significantly different in control and glutamate-treated cells (Table 3). The increase in intracellular Ca 2 + levels could result from the impairment of plasma membrane extrusion mechanisms, inhibition of sequestration by intracellular organelles or from the release of Ca 2 + from intracellular stores.…”

Section: Discussionmentioning

confidence: 66%

Oxidative glutamate toxicity involves mitochondrial dysfunction and perturbation of intracellular Ca2+ homeostasis

Pereira

Oliveira

2000

Neuroscience Research

143

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Glutamate toxicity on PC12 cells is mediated by oxidative stress as a consequence of the inhibition of a cystine uptake system with depletion of GSH. In this study we report that glutamate decreases PC12 cell viability, inhibiting the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). This decrease was prevented by the antioxidants vitamin E, idebenone and L-deprenyl, which were also shown to be effective in reducing the accumulation of reactive oxygen species (ROS) in cells exposed to glutamate, decreasing the fluorescence of 2%,7%-dichlorofluorescein (DCF). Incubation of PC12 cells with high glutamate concentrations induced mitochondrial dysfunction, leading to the loss of mitochondrial transmembrane potential, evaluated as a decrease in rhodamine 123 (Rh123) retention by mitochondria, and to the decrease of intracellular ATP levels. The mitochondrial dysfunction, induced by glutamate, can be involved in the observed increase of [Ca 2 + ] i . The elevation of [Ca 2 + ] i occurred after GSH depletion, suggesting that oxidative stress is involved in the disturbances of intracellular calcium homeostasis. In conclusion, our data indicate that glutamate, at concentrations which block cystine uptake in PC12 cells leading to GSH depletion and inducing oxidative stress, increases ROS accumulation and decreases cell survival by a mechanism involving mitochondrial dysfunction and impairment of Ca 2 + homeostasis.

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“…Previous work by other investigators and by using different biological preparations, is consistent with our results (Palmeira et. al., 1993;Pereira et. al., 1996;Tretter and Vizi 1996).…”

Section: Discussionmentioning

confidence: 94%

Lipid peroxidation and aluminium effects on the cholinergic system in nerve terminals

2001

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In the present study, we analyzed how aluminium and oxidative stress induced by ascorbate/Fe(2+) affect the mechanisms related with the cholinergic system in a crude synaptosomal fraction isolated from rat brain. [(3)H]Choline uptake, [(3)H]acetylcholine release, membrane potential and Na(+)/K(+)-ATPase activity were determined in the presence or in the absence of aluminium in control conditions and in the presence of ascorbate (0.8 mM)/Fe(2+) (2.5 micro M). The extent of lipid peroxidation was measured by quantifying thiobarbituric acid reactive substances (TBARS). Under oxidizing conditions aluminium increased the formation of TBARS by about 30%, but was without effect when the synaptosomal preparation was incubated in the absence of oxidants. Additionally, aluminium potentiated the inhibition of the high-affinity [(3)H]choline uptake observed following lipid peroxidation and had the same effect on the Na(+)/K(+)-ATPase activity. [(3)H]Acetylcholine release induced by 4-aminopyridine, and membrane potential were not significantly affected under oxidizing conditions, either in the absence or in the presence of aluminium. We can conclude that aluminium, by potentiating lipid peroxidation, affects the uptake of choline in nerve endings. This effect, occurring during brain oxidative injury, might contribute to the cholinergic dysfunction and neuronal cell degeneration known to occur in Alzheimer's disease.

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Contribution of plasma membrane and endoplasmic reticulum Ca2+-ATPases to the synaptosomal [Ca2+]i increase during oxidative stress

Cited by 38 publications

References 51 publications

Effects of H2O2 at rat myenteric neurones in culture

Effects of H2O2 at rat myenteric neurones in culture

Oxidative glutamate toxicity involves mitochondrial dysfunction and perturbation of intracellular Ca2+ homeostasis

Lipid peroxidation and aluminium effects on the cholinergic system in nerve terminals

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