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ISSN: 1734-1922
Archives of Medical Science
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4/2020
vol. 16
 
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Oncology
abstract:
Letter to the Editor

Arachidonic and eicosapentaenoic acids induce oxidative stress to suppress proliferation of human glioma cells

Anasuya Devi Hari
1
,
Naidu G. Vegi
2
,
Undurti N. Das
3

1.
BioScience Research Centre, GVP College of Engineering Campus, Visakhapatnam, India
2.
NIPER, Hyderabad, India
3.
UND Life Sciences, USA
Arch Med Sci 2020; 16 (4): 974–983
Online publish date: 2020/01/15
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Introduction

The most malignant tumor of the brain is glioblastoma multiforme (commonly called gliomas). Despite debulking surgery, radiation and chemotherapy, the survival of patients diagnosed to have glioblastoma multiforme is not more than 44 weeks. Gliomas are difficult to treat, partly because while growing they merge with normal brain tissue and hence during surgery it is difficult to delineate the tumor tissue from normal brain tissue to excise them completely. In view of this, developing newer therapeutic strategies that target glioma cells selectively with minimal toxicity to normal brain cells is urgently needed. Previous studies performed by us and others revealed that polyunsaturated fatty acids (PUFAs), especially -linolenic acid (GLA, 18:3 n-6), arachidonic acid (AA, 20:4 n-6), eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3), have selective tumoricidal action and induce apoptosis of glioma cells both in vitro and in vivo [1–7].
Previous studies revealed that many tumor cells have decreased expression of 6 and ∆5 desaturases that are essential for the formation of long-chain metabolites of dietary essential fatty acids (EFAs): linoleic (LA, 18:2 n-6) and -linolenic (ALA, 18:3 n-3) acids. This decrease in the activity of desaturases results in a deficiency of long-chain metabolites of EFAs such as GLA, dihomo-GLA (DGLA, 20:3 n-6), AA formed from LA and EPA and DHA from ALA in the tumor cells, possibly to protect themselves (tumor cells) from the cytotoxic action of PUFAs, free radicals (generated during the metabolism of EFAs/PUFAs) and lipid peroxides derived from various PUFAs [reviewed in 8, 9]. In a previous preliminary open label clinical study, we showed that intratumoral infusion/injection of GLA regresses glioblastoma [3, 4, 6] suggesting that some PUFAs can be exploited for the therapy of cancer including gliomas. This assumption is supported by the studies performed in cell cultures, rodent glioma and other tumor models, and preliminary human studies [1–19].
The tumoricidal action of various PUFAs has been attributed to their ability to enhance free radical generation and lipid peroxides specifically in tumor cells, changes in the lipid content of the cell membrane due to the incorporation of supplemented PUFA, action on anti-angiogenic factors and enzymes involved in lipid metabolism, changes in P-glycoprotein expression and induction of changes in...


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