The Effect of Mild and Severe Hypoxia on Rat Cortical Synaptosomes

Aldinucci, Carlo; Carretta, A.; Pessina, G. P.

doi:10.1007/s11064-005-6529-9

Cited by 7 publications

(7 citation statements)

References 32 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, isoprostanes, which are more chemically and metabolically stable, are good in vivo biomarkers of oxidative damage [36]. Accordingly we demonstrated that synaptosomes, which are pinched off resealed isolated nerve terminals prepared from cortical brain neurons containing essentially mitochondria, enzymes and vesicles of neurotransmitters, are very susceptible to oxidants and to hypoxia [38,39].…”

Section: Discussionmentioning

confidence: 82%

The Effects of Hypoxia/Reoxygenation on the Physiological Behaviour of U373-Mg Astrocytes

et al. 2009

View full text Add to dashboard Cite

Nerve cells are very susceptible to hypoxia responsive for mitochondrial dysfunctions involved in the subsequent oxidative stress, apoptosis and necrosis. In this paper, we examined the effect of 12 h incubation of U-373 MG astrocytes in hypoxic environment (73% N 2 : 2% O 2 : 5% CO 2 , v:v) by evaluating cell proliferation, modifications of NO and ATP production, intracellular Ca 2? concentration [Ca 2? ] i , membrane potential, desferoxaminechelatable free iron, esterified F2-isoprostanes levels and the production of phosphorylated ERK. The same parameters were evaluated also after a following re-oxygenation period of 24 h. Immediately after hypoxia the NO concentration increased significantly and returned to values similar to those of controls after the re-oxygenation period. At the same time, ATP levels remained similar to controls and the cell proliferation significantly decreased. This involved a significant increase of [Ca 2? ] i immediately after hypoxia and the value remained significantly elevated after the following re-oxygenation period. Moreover, after hypoxia, astrocytes were slightly although not significantly depolarized. Indeed iron and F2-isoprostanes levels increased significantly after hypoxia. Finally ERK proteins increased slowly and not significantly after hypoxia and the same trend was observed after the re-oxygenation period.On the whole, our results indicate that 2% O 2 hypoxia induces a moderate oxidative stress, well tolerated by U-373 MG cells, remaining the ATP production, mitochondrial membrane potential and activated ERK proteins, similar to the values of controls.

show abstract

Section: Discussionmentioning

confidence: 82%

The Effects of Hypoxia/Reoxygenation on the Physiological Behaviour of U373-Mg Astrocytes

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Synaptosomes are nerve terminals prepared from gently homogenized brain, which reseal after separation from the nerve fibres; they possess many of the properties of the synapses. We used cortical synaptosomes because mitochondria from different tissues have different susceptibility to physical stress and neuronal mitochondria are more vulnerable to oxidants than astrocytic mitochondria [Aldinucci et al, 2005].…”

Section: Discussionmentioning

confidence: 99%

Synaptosome behaviour is unaffected by weak pulsed electromagnetic fields

Aldinucci

Carretta

Maiorca

et al. 2007

Bioelectromagnetics

Self Cite

View full text Add to dashboard Cite

The present study examined the effect on rat cortical synaptosomes of a 2 h exposure to 50-Hz electromagnetic fields (EMFs) with a peak magnetic field of 2 mT. We measured modifications of synaptosomal mitochondrial respiration rate, ATP production, membrane potential, intrasynaptosomal Ca(2+) concentration and free iron release. The O(2) consumption remained unvaried in exposed synaptosomes at about 2 nM O(2)/min/mg proteins; ATP production was also unchanged. The intrasynaptosomal Ca(2+) concentration decreased slowly and there was a slight, but non-significant, depolarisation of the synaptosomal membrane. Finally, the free iron release by synaptosomal suspensions, a useful predictor of neuro-developmental outcome, remained unchanged after EMF exposure. On the whole, our results indicate that the physiological behaviour of cortical synaptosomes is not affected by weak pulsed EMFs.

show abstract

“…The release of free iron and the production of protein carbonyls, 4 hydroxynonenal (4HNE) protein adducts and F 2 -isoprostanes after hypoxia are closely correlated, as demonstrated by our previous paper [11], and are all highly accurate quantitative markers of oxidative stress [12]. Moreover, we have demonstrated that synaptosomes (pinched off and resealed isolated nerve terminals prepared from cortical brain neurons and essentially containing mitochondria, enzymes and vesicles of neurotransmitters) are very susceptible to oxidants and to hypoxia [13,14].…”

Section: Introductionmentioning

confidence: 83%

The Physiological Behaviour of IMR-32 Neuroblastoma Cells is Affected by a 12-h Hypoxia/24-h Reoxygenation Period

et al. 2010

View full text Add to dashboard Cite

Nervous system cells are highly dependent on adequate tissue oxygenation and are very susceptible to hypoxia, which causes mitochondrial dysfunctions involved in apoptosis and necrosis. In this paper, we examine the effect of a 12-h incubation of differentiated IMR-32 neuroblastoma cells in a hypoxic environment (73% N(2): 2% O(2): 5% CO(2), v:v) by evaluating cell viability, modifications of NO, intracellular Ca(2+) concentration [Ca(2+)](i) and membrane potential, the production of phosphorylated ERK, desferoxamine-chelatable free iron and esterified F2-isoprostane levels. The same parameters were evaluated after a subsequent 24-h re-oxygenation period. The NO concentration increased significantly immediately after hypoxia and returned to values similar to those of controls after the reoxygenation period. At the same time, we observed a significant increase of [Ca(2+)](i) immediately after hypoxia. Phosphorylated ERK proteins increased significantly during the first 2 h of hypoxia, then decreased, and remained practically unmodified after 12 h hypoxia and the following reoxygenation period. Moreover, IMR-32 cell mitochondria were significantly depolarized after hypoxia, while membrane potential returned to normal after the reoxygenation period. Finally, desferoxamine-chelatable free iron and F2-isoprostane levels also increased significantly after hypoxia. Our results indicate that 2% O(2) hypoxia induces variations of NO and [Ca(2+)](i) with subsequent mitochondrial depolarization, and it is responsible for oxidative stress, represented by increased free iron and F2-isoprostane, protein carbonyls and 4 hydroxynonenal protein adducts levels.

show abstract

The Effect of Mild and Severe Hypoxia on Rat Cortical Synaptosomes

Cited by 7 publications

References 32 publications

The Effects of Hypoxia/Reoxygenation on the Physiological Behaviour of U373-Mg Astrocytes

The Effects of Hypoxia/Reoxygenation on the Physiological Behaviour of U373-Mg Astrocytes

Synaptosome behaviour is unaffected by weak pulsed electromagnetic fields

The Physiological Behaviour of IMR-32 Neuroblastoma Cells is Affected by a 12-h Hypoxia/24-h Reoxygenation Period

Contact Info

Product

Resources

About