Role of membrane lipid oxidation in control of enzymatic activity in normal and cancer cells

Burlakova, E. B.; Molochkina, E. M.; Palmina, N. P.

doi:10.1016/0065-2571(80)90014-x

Cited by 16 publications

(4 citation statements)

References 10 publications

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“…A large body of work over many years has established that an increased rate of cell division is often associated with a decreased rate of lipid peroxidation, and this has led to the hypothesis that lipid peroxidation may be involved in the same mechanisms that influence cell division (Slater, 1976;Burlakova et al, 1980;Slater et al, 1984;Morisaki et al, 1984;Cheeseman et al, 1986a,b). The data presented here do not conflict with that general hypothesis.…”

Section: Measurementmentioning

confidence: 99%

Studies on lipid peroxidation in normal and tumour tissues. The Yoshida rat liver tumour

Cheeseman

Emery

Maddix

et al. 1988

Biochemical Journal

122

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Reduced rates of lipid peroxidation have been observed in Yoshida hepatoma cells and microsomes when compared with appropriate control tissue (normal rat liver) under the same pro-oxidant conditions. The pro-oxidant conditions used were incubation with NADPH+ADP+iron or ascorbate+iron or exposure to gamma-irradiation. As previously shown with the Novikoff hepatoma, the relative concentrations of alpha-tocopherol and polyunsaturated fatty acids are important in conferring resistance to lipid peroxidation in the Yoshida hepatoma. Furthermore, NADPH-cytochrome c reductase and the NADPH-cytochrome P-450 electron transport chain, which are involved in the initiation and propagation of certain types of lipid peroxidation, are found at very much reduced levels in the Yoshida hepatoma. The relative importance of these aberrations are discussed.

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Section: Measurementmentioning

confidence: 99%

Studies on lipid peroxidation in normal and tumour tissues. The Yoshida rat liver tumour

Cheeseman

Emery

Maddix

et al. 1988

Biochemical Journal

122

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“…Many studies have concluded that lipid peroxidation is significantly decreased in rat tumour cells and tissues compared with the corresponding normal tissues (see Utsumi et al, 1965;Lash, 1966;Fonnesu et al, 1966;Ugazio et al, 1968;Burlakova, 1975;Burlakova et al, 1980;Bartoli & Galeotti, 1979;Player et al, 1979;Dianzani et al, 1984;Sharma et al, 1984). However, it should be noted right at the outset that it is often difficult to obtain a completely satisfactory sample ofthe 'corresponding normal tissue'; indeed, with some tumours it is even unclear what is the corresponding normal tissue.…”

Section: Introductionmentioning

confidence: 99%

Studies on lipid peroxidation in normal and tumour tissues. The Novikoff rat liver tumour

Cheeseman¹,

Collins²,

Proudfoot³

et al. 1986

Biochemical Journal

132

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A study has been made of the factors that contribute to the decreased rates of lipid peroxidation under different pro-oxidant conditions in intact Novikoff tumour cells, and in microsomal suspensions prepared from Novikoff tumour cells, compared with isolated normal rat hepatocytes and microsomal suspensions prepared from normal rat liver. The pro-oxidant conditions were the addition of either NADPH, NADPH + ADP + iron, NADPH + CCl4 or ascorbate+iron to the experimental systems used, or exposure to gamma-radiation. Contributory factors to the lower rates of lipid peroxidation observed include: a significant decrease in the polyunsaturated fatty acid content of Novikoff cells or Novikoff microsomes; the decreases are especially marked for the C20:4 and C22:6 fatty acids; a very marked reduction in NADPH-cytochrome c reductase; and no detectable content of cytochrome P-450. Another, and in our opinion critical, contribution to the diminished rate of lipid peroxidation in the tumour material is the substantial increase in alpha-tocopherol relative both to total lipid and to methylene-interrupted double bonds in fatty acids. Moreover, the alpha-tocopherol is the major contributor to lipid-soluble chain-breaking antioxidant in lipid extracts of normal liver and of Novikoff tumour material.

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“…In normal conditions, membrane phospholipids are asymmetrically distributed across cell membrane monolayers, with phosphatidylserine (PS) and phosphatidylethanolamine (PE) located on inner face, and sphingomyeline (SM) and phosphatedylcholine (PC) on outer face [62,63]. Asymmetric distribution of lipids was also observed in plasma membrane of tumour cells, but with reversed localization for phosphatidylserine (PS), which is present on outer face [64]. Remarkably, numerous tumour cell lines have been reported to display 3-to 7-fold elevated amounts of PS on exoplasmic membrane leaflet compared with nontumorigenic cells [65].…”

Section: Discussionmentioning

confidence: 99%

Patatin-like PLA<sub>2</sub> with cytotoxicity against mammalian and plant tumour cells

Griffaut¹,

Débiton²,

Galmier³

et al. 2013

ABC

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Plants can respond to traumatism by synthesis and secretion of defence molecules. Wound-healing and desiccation stress of pieces of potato tuber parenchyma (Solanum tuberosum) promoted the secretion of a patatin-like phospholipase A 2 , PLA 2 (EC.3.1.1.4.) that displayed cytotoxic activity against tumour cells. The potato secretion product, an oligomeric form of patatin-like protein, was shown to contain several isoforms of PLA 2 polypeptides and to be associated with other proteins, including Kunitz-type protease inhibitors. Patatin-like protein secretion was inhibited by vanadate. Secreted patatin-like proteins displayed specific features, such as extracellular function and low molecular weights, mainly 36 to 40 kDa. The 36-kDa polypeptide sequence was related to iPLA 2 α. Polypeptide spots of secreted patatin-like protein exhibited a nucleotide-binding consensus motif, GGGIKG that has been described in iPLA 2 gene family. The cytotoxic agent caused cell death of plant crown-gall induced by Agrobacterium tumefaciens, and inhibited B16 cell proliferation, but at the same concentration did not display any toxicity against non-transformed cells. PLA 2 enzyme activity was required for cytotoxicity against B16 melanoma cells. A model for such a specific activity against tumour cells is discussed in connection with asymmetric phospholipid patterns of cell membranes. In conclusion, secreted patatin-like PLA 2 (e-patatin) may represent a novel therapeutic target for the development of new agents against cancer.

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Role of membrane lipid oxidation in control of enzymatic activity in normal and cancer cells

Cited by 16 publications

References 10 publications

Studies on lipid peroxidation in normal and tumour tissues. The Yoshida rat liver tumour

Studies on lipid peroxidation in normal and tumour tissues. The Yoshida rat liver tumour

Studies on lipid peroxidation in normal and tumour tissues. The Novikoff rat liver tumour

Patatin-like PLA<sub>2</sub> with cytotoxicity against mammalian and plant tumour cells

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Role of membrane lipid oxidation in control of enzymatic activity in normal and cancer cells

Cited by 16 publications

References 10 publications

Studies on lipid peroxidation in normal and tumour tissues. The Yoshida rat liver tumour

Studies on lipid peroxidation in normal and tumour tissues. The Yoshida rat liver tumour

Studies on lipid peroxidation in normal and tumour tissues. The Novikoff rat liver tumour

Patatin-like PLA&lt;sub&gt;2&lt;/sub&gt; with cytotoxicity against mammalian and plant tumour cells

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Product

Resources

About

Patatin-like PLA<sub>2</sub> with cytotoxicity against mammalian and plant tumour cells