TISSUE CULTURE AND THE STUDY OF ANTICANCER AGENTS

1966 ◽  
Vol 44 (2) ◽  
pp. 339-343 ◽  
Author(s):  
Susan Tolnai
Keyword(s):  
Fatty Acids ◽  
Tumor Cells ◽  
Anticancer Agents ◽  
Antitumor Agents ◽  
Unsaturated Fatty Acids ◽  
Ascites Tumor ◽  
Mouse Tumors ◽  
Arachidonic Acids

In a quest for potential antitumor agents, more than 100 fatty acids and their derivatives were tested against transplantable mouse tumors with both in vivo and in vitro methods. Three compounds, 2,3-decenoic acid, linoleic acid, and linolenic acid, were found to arrest the growth of three types of ascites tumor cells, while 2-nonenoic, 10-undecenoic, oleic, and arachidonic acids were effective to a varying degree. The cytotoxic effects of these unsaturated fatty acids on monolayer cultures of Ehrlich ascites tumor cells and of normal mouse embryos were evaluated in experiments in which graded concentrations of the test materials incorporated in the culture medium were used.

Glucose-stimulated acrolein production from unsaturated fatty acids

2004 ◽  
Vol 23 (2) ◽  
pp. 101-105 ◽  
Author(s):  
R Medina-Navarro ◽  
G Duran-Reyes ◽  
M Diaz-Flores ◽  
J J Hicks ◽  
J Kumate R
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Tissue Injury ◽  
Acid Product ◽  
Hydroperoxide Formation ◽  
Fatty Acid Product ◽  
Arachidonic Acids

Glucose auto-oxidation may be a significant source of reactive oxygen species (ROS), and also be important in the lipid peroxidation process, accompanied by the release of toxic reactive products. We wanted to demonstrate that acrolein can be formed directly and actively from free fatty acids in a hyperglycemic environment. A suspension of linoleic and arachidonic acids (2.5 mM) was exposed to different glucose concentrations (5, 10 and 15 mmol/L) in vitro. The samples were extracted with organic solvents, partitioned, followed at 255 / 267 nm, and analysed using capillary electrophoresis and mass spectroscopy. The total release of aldehydes significantly (P ≤ 0.01) increased from 1.0 to 5.1, 8.3 and 13.1 μmol/L after 6 hours of incubation, proportional to glucose concentrations. It was possible to verify a correlate hydroperoxide formation as well. Among the lipid peroxidation products, acrolein (5% of total) and its condensing product, 4-hydroxy-hexenal, were identified. From the results presented here, it was possible to demonstrate the production of acrolein, probably as a fatty acid product, due to free radicals generated from the glucose auto-oxidation process. The results led us to propose that acrolein, which is one of the most toxic aldehydes, is produced during hyperglycemic states, and may lead to tissue injury, as one of the initial problems to be linked to high levels of glucose in vivo.

In vitro and in vivo inhibition of renin by fatty acids.

1978 ◽  
Vol 234 (6) ◽  
pp. E593 ◽  
Author(s):  
T A Kotchen ◽  
W J Welch ◽  
R T Talwalkar
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Linoleic Acid ◽  
Angiotensin Ii ◽  
Neutral Lipids ◽  
Pressor Response ◽  
Arterial Blood ◽  
Arachidonic Acids

Circulating neutral lipids inhibit the in vitro renin reaction. To identify the inhibitor(s), free fatty acids were added to human renin and homologous substrate. Capric, lauric, palmitoleic, linoleic, and arachidonic acids each inhibited the rate of angiotensin I production in vitro (P less than 0.01). Inhibition by polysaturated fatty acids (linoleic and arachidonic) was less (P less than 0.01) after catalytic hydrogenation of the double bonds. To evaluate an in vivo effect of renin inhibition intra-arterial blood pressure responses to infusions of renin and angiotensin II (5.0 microgram) were measured in anephric rats (n = 6) before and after infusion of linoleic acid (10 mg iv). Mean increase of blood pressure to angiotensin II before (75 mmHg +/- 9) and after (90 +/- 12) linoleic acid did not differ (P greater than 0.05). However, the pressor response to renin after linoleic acid (18 +/- 3) was less (P less than 0.00)) than that before (102 +/- 13). In summary, several fatty acids inhibit the in vitro renin reaction, and in part inhibition is dependent on unsaturation. Linoleic acid also inhibits the in vivo pressor response to renin. These results suggest that fatty acids may modify the measurement of plasma renin activity and may also affect angiotensin production in vivo.

The Effect of Fatty Acids upon Tumor Cell Respiration and Transplantability

1963 ◽  
Vol 9 (5) ◽  
pp. 530-543 ◽  
Author(s):  
Bernard J Katchman ◽  
Robert E Zipf ◽  
James P F Murphy
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Tumor Cells ◽  
Chemical Structure ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Leukemic Cells ◽  
Endogenous Respiration ◽  
Low Concentrations

Abstract The kinetic effect of palmitate, stearate, oleate, linoleate, and linolenate upon in vitro endogenous respiration of rat chloromyeloid leukemic cells has been investigated. Inhibition of respiration has been correlated with the ability of fatty acids to cause decreased cell viability and cell count; in the bioassay of fatty acid-treated tumor inocula, the increase in animal life span is correlated to the degree of dilution of the inocula due to cell lysis. The degree of lysis is dependent upon the chemical structure of the fatty acid, concentration, and duration of contact; unsaturated fatty acids are more effective than saturated fatty acids. Tumor cells, when incubated at low concentrations of fatty acids, show stimulation of O2 uptake; however, in the bioassay these fatty acid-treated inocula showed no loss in tumor activity. The nature of the physiochemical interaction between fatty acids and tumor cells is discussed.

In vitro and in vivo fate of saturated and unsaturated fatty acids during development of insects

1974 ◽  
Vol 360 (3) ◽  
pp. 289-297 ◽  
Author(s):  
A.M. Municio ◽  
J.M. Odriozola ◽  
M.A. Pérez-Albarsanz ◽  
J.A. Ramos
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids

[10]-Gingerol Affects Multiple Metastatic Processes and Induces Apoptosis in MDAMB- 231 Breast Tumor Cells

2019 ◽  
Vol 19 (5) ◽  
pp. 645-654 ◽  
Author(s):  
Angelina M. Fuzer ◽  
Ana C.B.M. Martin ◽  
Amanda B. Becceneri ◽  
James A. da Silva ◽  
Paulo C. Vieira ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Antitumor Agents ◽  
Apoptotic Cell ◽  
3D Culture ◽  
Primary Concern ◽  
Breast Cancers ◽  
Her2 Gene

Background: Triple Negative Breast Cancer (TNBC) represents the approximately 15% of breast cancers that lack expression of Estrogen (ER) and Progesterone Receptors (PR) and do not exhibit amplification of the human epidermal growth factor receptor 2 (HER2) gene, imposing difficulties to treatment. Interactions between tumor cells and their microenvironment facilitate tumor cell invasion in the surrounding tissues, intravasation through newly formed vessels, and dissemination to form metastasis. To treat metastasis from breast and many other cancer types, chemotherapy is one of the most extensively used methods. However, its efficacy and safety remain a primary concern, as well as its toxicity and other side effects. Thus, there is increasing interest in natural antitumor agents. In a previous work, we have demonstrated that [10]-gingerol is able to revert malignant phenotype in breast cancer cells in 3D culture and, moreover, to inhibit the dissemination of TNBC to multiple organs including lung, bone and brain, in spontaneous and experimental in vivo metastasis assays in mouse model. Objective: This work aims to investigate the in vitro effects of [10]-gingerol, using human MDA-MB-231TNBC cells, in comparison to non-tumor MCF-10A breast cells, in order to understand the antitumor and antimetastatic effects found in vivo and in a 3D environment. Methods: We investigated different steps of the metastatic process in vitro, such as cell migration, invasion, adhesion and MMP activity. In addition, we analyzed the anti-apoptotic and genotoxic effects of [10]-gingerol using PEAnnexin, DNA fragmentation, TUNEL and comet assays, respectively. Results: [10]-gingerol was able to inhibit cell adhesion, migration, invasion and to induce apoptosis more effectively in TNBC cells, when compared to non-tumor cells, demonstrating that these mechanisms can be involved in the antitumor and antimetastatic effects of [10]-gingerol, found both in 3D culture and in vivo. Conclusion: Taken together, results found here are complementary to previous studies of our group and others and demonstrate that additional mechanisms, besides apoptotic cell death, is used by [10]-gingerol to accomplish its antitumor and antimetastatic effects. Our results indicate a potential for this natural compound as an antitumor molecule or as an adjuvant for chemotherapeutics already used in the clinic.

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