Some effects of the essential fatty acids linoleic acid and alpha-linolenic acid and of their metabolites gamma-linolenic acid, arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and of prostaglandins A1 and E1 on the proliferation of human osteogenic sarcoma cells in culture

Booyens, J; Engelbrecht, P; Roux, Sylvain; Louwrens, C.C.; Merwe, C.F. van der; Katzeff, I.E.

doi:10.1016/0262-1746(84)90053-2

Cited by 81 publications

(22 citation statements)

References 3 publications

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“…Nevertheless, these results are far from conclusive. For instance, one study found that linoleic acid (C18:2 n-6 PUFA) suppressed cancer cell proliferation [Booyens et al, 1984], while other studies indicate an enhancing effect on carcinogenesis [Appel et al, 1994;Johanning and Lin, 1995;Newcomer et al, 2001]. Oleic acid (C18:1, n-9 MUFA), a promoter of cancer cell proliferation [Booyens et al, 1984], has been reported to be an effective anticancer and antimutagenic agent [Siegel et al, 1987;Iwado et al, 1991].…”

Section: Introductionmentioning

confidence: 99%

“…Oleic acid (C18:1, n-9 MUFA), a promoter of cancer cell proliferation [Booyens et al, 1984], has been reported to be an effective anticancer and antimutagenic agent [Siegel et al, 1987;Iwado et al, 1991]. Linolenic acid (C18:3 short-chain n-3 PUFA) had anticancer activity in some studies [Booyens et al, 1984;Bégin et al, 1985], but promoted cancer in other studies [Ramon et al, 2000;Newcomer et al, 2001].…”

Section: Introductionmentioning

confidence: 99%

“…For instance, one study found that linoleic acid (C18:2 n-6 PUFA) suppressed cancer cell proliferation [Booyens et al, 1984], while other studies indicate an enhancing effect on carcinogenesis [Appel et al, 1994;Johanning and Lin, 1995;Newcomer et al, 2001]. Oleic acid (C18:1, n-9 MUFA), a promoter of cancer cell proliferation [Booyens et al, 1984], has been reported to be an effective anticancer and antimutagenic agent [Siegel et al, 1987;Iwado et al, 1991]. Linolenic acid (C18:3 short-chain n-3 PUFA) had anticancer activity in some studies [Booyens et al, 1984;Bégin et al, 1985], but promoted cancer in other studies [Ramon et al, 2000;Newcomer et al, 2001].…”

Section: Introductionmentioning

confidence: 99%

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Genotoxicity of vegetable cooking oils in the Drosophila wing spot test

Rojas-Molina

Campos-Sánchez

Analla

et al. 2004

Environ. Mol. Mutagen.

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Seven vegetable oils consumed by humans were tested for genotoxic activity in the Drosophila somatic mutation and recombination test. The oils included five seed oils (sesame, sunflower, wheat germ, flax, and soy oil) and both first-class extra-virgin and low-grade (refined) olive oil. Larvae of the standard (STD) and highly bioactive (NORR) crosses of Drosophila melanogaster were fed medium containing 6% and 12% of each of the oils. Flax oil produced the strongest response, while sesame, wheat germ, and soy oil showed some genotoxic activity. Sunflower and the low-grade olive oil gave inconclusive results, and extra-virgin olive oil was clearly nongenotoxic. It is argued that the genotoxicity is probably due to the fatty acid composition of the oils, which after peroxidation can form specific DNA-adducts.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Genotoxicity of vegetable cooking oils in the Drosophila wing spot test

Rojas-Molina

Campos-Sánchez

Analla

et al. 2004

Environ. Mol. Mutagen.

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“…Alpha-linolenic acid (ALA, 18-carbon unsaturated fatty acid obtained from plant sources), eicosapentaenoic acid (EPA, 20-carbon unsaturated fatty acid obtained from marine source), and docosahexaenoic acid (DHA, 22-carbon unsaturated fatty acid obtained from marine source) are well-known omega-3 FAs which play an important role in human physiology [28][29][30]. Our body has a limited ability to form EPA and DHA from ALA [31,32].…”

Section: Introductionmentioning

confidence: 99%

Omega-3 polyunsaturated fatty acids and cancer: lessons learned from clinical trials

Nabavi

Bilotto

Russo

et al. 2015

Cancer Metastasis Rev

139

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Over the past decades, extensive studies have addressed the therapeutic effects of omega-3 polyunsaturated fatty acids (omega-3 FAs) against different human diseases such as cardiovascular and neurodegenerative diseases, cancer, etc. A growing body of scientific research shows the pharmacokinetic information and safety of these natural occurring substances. Moreover, during recent years, a plethora of studies has demonstrated that omega-3 FAs possess therapeutic role against certain types of cancer. It is also known that omega-3 FAs can improve efficacy and tolerability of chemotherapy. Previous reports showed that suppression of nuclear factor-κB, activation of AMPK/SIRT1, modulation of cyclooxygenase (COX) activity, and up-regulation of novel anti-inflammatory lipid mediators such as protectins, maresins, and resolvins, are the main mechanisms of antineoplastic effect of omega-3 FAs. In this review, we have collected the available clinical data on the therapeutic role of omega-3 FAs against breast cancer, colorectal cancer, leukemia, gastric cancer, pancreatic cancer, esophageal cancer, prostate cancer, lung cancer, head and neck cancer, as well as cancer cachexia. We also discussed the chemistry, dietary source, and bioavailability of omega-3 FAs, and the potential molecular mechanisms of anticancer and adverse effects.

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“…The earliest studies appeared in the 1980s and many additional reports have confirmed and extended this general finding during the past 25 years [2][3][4][5]. Initially, research was directed towards tumour cell lines such as breast and colon cancer for which epidemiological data suggested a link between dietary fat intake and cancer incidence.…”

Section: Fatty Acid Effects On Tumour Cell Proliferationmentioning

confidence: 91%

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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Some effects of the essential fatty acids linoleic acid and alpha-linolenic acid and of their metabolites gamma-linolenic acid, arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and of prostaglandins A1 and E1 on the proliferation of human osteogenic sarcoma cells in culture

Cited by 81 publications

References 3 publications

Genotoxicity of vegetable cooking oils in the Drosophila wing spot test

Genotoxicity of vegetable cooking oils in the Drosophila wing spot test

Omega-3 polyunsaturated fatty acids and cancer: lessons learned from clinical trials

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

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