Comparative anti-mitotic effects of lithium gamma-linolenate, gamma-linolenic acid and arachidonic acid, on transformed and embryonic cells

Seegers, J.C.; Lottering, Mona-Liza; Panzer, Annie; Bianchi, Pepita; Stark, J. H.

doi:10.1016/s0952-3278(98)90143-0

Cited by 5 publications

(4 citation statements)

References 10 publications

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“…Our results thus show that linoleic acid can induce apoptosis in hybridoma cells. This is in accordance with some recent studies showing that apoptosis can be induced by PUFAs from the o-6 family, like arachidonic acid and gamma-linolenic acid (Chen et al, 1997;de Kock et al, 1996;Seegers et al, 1997Seegers et al, , 1998.…”

Section: Apoptosis Measurementssupporting

confidence: 93%

Application of a continuous bioreactor cascade to study the effect of linoleic acid on hybridoma cell physiology

Kisztelinski

Alink

Rietjens

et al. 2006

Biotechnol. Bioeng.

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The aim of the present study is to demonstrate the use of controlled bioreactors for toxicological studies. As a model system the effect of linoleic acid on hybridoma cells is studied in two well-controlled continuously operated bioreactors placed in series. In the first reactor the effect on rapid proliferating cells can be studied, while in the second reactor a special steady state is created, which allows studying the effect on apoptotic cells. Experiments are done at 0, 25, and 50 microM linoleic acid. At the end of the experiment with 50 microM linoleic acid, the concentration of linoleic acid is increased stepwise to determine the cytotoxic level. For rapid proliferating cells exposed to 25 and 50 microM stimulation of growth was observed. At 50 microM there was at the same time an increase in cell death through apoptosis. For stressed apoptotic cells linoleic acid caused partial growth inhibition at 25 and 50 microM and arrest of cell proliferation in the G(2)/M phase at 50 microM. For both, rapid proliferating cells and stressed apoptotic cells, complete growth inhibition occurred at 85 microM, with cells being arrested in the G(2)/M phase and dying mainly through necrosis. Cells in the bioreactor system appeared to be more sensitive towards linoleic acid than cells grown in multi-well plates. (IC(50) = 300 microM; IC(100) = 400 microM). Altogether the results of the present study reveal that the biostat experiments allow detailed analysis of the effect of a bioactive ingredient on cell physiology and behavior.

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Section: Apoptosis Measurementssupporting

confidence: 93%

Application of a continuous bioreactor cascade to study the effect of linoleic acid on hybridoma cell physiology

Kisztelinski

Alink

Rietjens

et al. 2006

Biotechnol. Bioeng.

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“…Interestingly, in this model, EPA caused a higher rate of TBARS production along with a greater inhibition of tumour growth in vivo than the more unsaturated DHA. Both GLA and AA inhibited the cell cycle in various other tumour cells causing reductions in S-phase and induction of apoptosis [71][72][73]. DHA has also been reported to exert similar effects in leukaemia cells with S-phase cycle arrest, increased p21 expression and increased pro-caspase-3 cleavage leading to increased apoptotic rate [74,75].…”

Section: Fatty Acid Induction Of Cell Deathmentioning

confidence: 92%

Lipids, Mitochondria and Cell Death: Implications in Neuro-oncology

Colquhoun

2010

Mol Neurobiol

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Polyunsaturated fatty acids (PUFAs) are known to inhibit cell proliferation of many tumour types both in vitro and in vivo. Their capacity to interfere with cell proliferation has been linked to their induction of reactive oxygen species (ROS) production in tumour tissues leading to cell death through apoptosis. However, the exact mechanisms of action of PUFAs are far from clear, particularly in brain tumours. The loss of bound hexokinase from the mitochondrial voltage-dependent anion channel has been directly related to loss of protection from apoptosis, and PUFAs can induce this loss of bound hexokinase in tumour cells. Tumour cells overexpressing Akt activity, including gliomas, are sensitised to ROS damage by the Akt protein and may be good targets for chemotherapeutic agents, which produce ROS, such as PUFAs. Cardiolipin peroxidation may be an initial event in the release of cytochrome c from the mitochondria, and enriching cardiolipin with PUFA acyl chains may lead to increased peroxidation and therefore an increase in apoptosis. A better understanding of the metabolism of fatty acids and eicosanoids in primary brain tumours such as gliomas and their influence on energy balance will be fundamental to the possible targeting of mitochondria in tumour treatment.

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“…[371][372][373][374] There is evidence that Li-GLA has a substantial antitumor effect in a range of cancers. [375][376][377][378] It may be that the cytotoxicity of the Li-GLA salt is a combination of the separate and individual effects of the essential fatty acid and the lithium ion. Clinical trials are under way in pancreatic cancer, a particularly aggressive tumor with relatively short survival time in normal circumstances.…”

Section: E Oncologymentioning

confidence: 99%

“…The lithium salt of gamma linolenic acid (LiGLA) has been assessed for its effects on the reduction of progression of a range of cancers following the demonstration of cytotoxicity by gamma linolenic acid and its salts, in vitro, toward a range of malignant cells. − There is evidence that Li−GLA has a substantial antitumor effect in a range of cancers. − It may be that the cytotoxicity of the Li−GLA salt is a combination of the separate and individual effects of the essential fatty acid and the lithium ion. Clinical trials are under way in pancreatic cancer, a particularly aggressive tumor with relatively short survival time in normal circumstances. ,, …”

Section: E Oncologymentioning

confidence: 99%

Inorganic Pharmacology of Lithium

Birch¹

1999

Chem. Rev.

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Comparative anti-mitotic effects of lithium gamma-linolenate, gamma-linolenic acid and arachidonic acid, on transformed and embryonic cells

Cited by 5 publications

References 10 publications

Application of a continuous bioreactor cascade to study the effect of linoleic acid on hybridoma cell physiology

Application of a continuous bioreactor cascade to study the effect of linoleic acid on hybridoma cell physiology

Lipids, Mitochondria and Cell Death: Implications in Neuro-oncology

Inorganic Pharmacology of Lithium

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