Clastogenic and cytotoxic effects of spermine oxidation products in mouse lymphoma L5178Y cells

Boużyk, Elżbieta; Rosiek, O

doi:10.1016/0304-3835(88)90044-4

Cited by 8 publications

(6 citation statements)

References 17 publications

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“…There have been several reports on the role of H202, oxygen radicals and oxidative stress in polyamine-induced toxicity in the presence of bovine serum amine oxidase. Inhibition of lymphocyte proliferation was independent of exogenously added catalase [24], whereas spermidine toxicity in CHO cells was decreased by the presence of catalase [46], as was the clastogenic effect of spermine in mouse lymphoma cells [47]. Studies using exogenous catalase are difficult to interpret, as the enzyme is a known constituent of serum, and its activity will vary between sera and different batches of the same serum.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of spermine toxicity in baby-hamster kidney (BHK) cells. The role of amine oxidases and oxidative stress

Brunton

Grant

Wallace

1991

Biochemical Journal

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Spermine was toxic to BHK-21/C13 cells in the absence of any extracellular metabolism of the amine. Inhibition of copper-containing amine oxidases with aminoguanidine partially prevented the response, whereas inhibition of polyamine oxidase with MDL-72,527 exacerbated the effect. Oxidation by an intracellular copper-containing amine oxidase may be involved in the toxicity of spermine, whereas the polyamine-interconversion pathway appears to play a cytoprotective role. There was no evidence for spermine imposing a state of oxidative stress within the cells. Inhibition of catalase and glutathione reductase did not alter the cytotoxicity of spermine, and there was no excretion of oxidized glutathione into the extracellular medium. The results suggest that spermine itself can exert a toxic effect directly on the cells.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of spermine toxicity in baby-hamster kidney (BHK) cells. The role of amine oxidases and oxidative stress

Brunton

Grant

Wallace

1991

Biochemical Journal

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“…3‐aminopropanal, 3‐AP, is highly toxic at rather low concentrations to a variety of cells, including neurons, glial cells, endothelial cells, fibroblasts, and a range of transformed mammalian cell types (6, 32, 33). The exact mechanisms behind the pronounced cytotoxicity of this small amino aldehyde, however, are not yet generally realized.…”

Section: Discussionmentioning

confidence: 99%

3‐Aminopropanal is a lysosomotropic aldehyde that causes oxidative stress and apoptosis by rupturing lysosomes

Li²,

Brunk³

2003

APMIS

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During cerebral ischemia and following trauma, potent cytotoxic polyamine-derived aminoaldehydes form, diffuse, and damage adjacent tissues not directly subjected to the initial insult. One such aldehyde is 3-aminopropanal (3-AP). The mechanisms by which such a small aldehydic compound is excessively cytotoxic have been unclear until recently when we showed that 3-AP, having the structure of a weak lysosomotropic base, concentrates within the acidic vacuolar compartment and causes lysosomal rupture that, in turn, induces caspase activation and apoptotic cell death. Here, using cultured J774 cells and 3-AP as a way to selectively burst lysosomes, we show that moderate lysosomal rupture induces a transient wave of oxidative stress. The start of this oxidative stress period is concomitant with a short period of enhanced mitochondrial membrane potential that later fades and is replaced by a decreased potential before the oxidative stress diminishes. The result of the study suggests that oxidative stress, which has often been described during apoptosis induced by agonists other than oxidative stress per se, may be a consequence of lysosomal rupture with direct and/or indirect effects on mitochondrial respiration and electron transport causing a period of passing enhanced formation of reactive oxygen species.

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“…3-Aminopropanal was previously implicated as cytotoxic and cytostatic to primary endothelial cells, fibroblasts, and other transformed mammalian cell lines in culture [54][55][56][57][58]. Toverify that 3-aminopropanal is generated by oxidative cleavage of spermine and spermidine by PAO, we used stereotactic microinjection methods to administer spermine, spermidine, and putrescine into the cerebral cortex of rats and then measured the volume of tissue death that developed at the injection site.Spermine and spermidine, but not putrescine, mediated significant cortical brain cell death [18].…”

Section: -Aminopropanal As a Mediator In Cerebral Ischemiamentioning

confidence: 99%

Polyamine Oxidase and 3-Aminopropanal in the Pathogenesis of Cerebral Ischemia

Ivanova

Czura

Tracey

2002

Mechanisms of Organ Dysfunction in Critical Illness

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Clastogenic and cytotoxic effects of spermine oxidation products in mouse lymphoma L5178Y cells

Cited by 8 publications

References 17 publications

Mechanisms of spermine toxicity in baby-hamster kidney (BHK) cells. The role of amine oxidases and oxidative stress

Mechanisms of spermine toxicity in baby-hamster kidney (BHK) cells. The role of amine oxidases and oxidative stress

3‐Aminopropanal is a lysosomotropic aldehyde that causes oxidative stress and apoptosis by rupturing lysosomes

Polyamine Oxidase and 3-Aminopropanal in the Pathogenesis of Cerebral Ischemia

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