Effect on DNA synthesis in LLC

Therefore, we compared the tumor cytotoxicity between EPA ethylester and the accelerated test-formed by-products in in vitro models. The inhibitory effects of E-1 (EPA ethylester dimer) and E-2 (EPA hydroxyethylester) isolated from EPAD on DNA synthesis in LLC cells were stronger than those of EPA ethylester Fig. (9) . Furthermore, it was found that the effects of E-1 (EPA ethylester... 

To characterize the antitumor and/or antimetastatic activities, the effects of carp oil and oleic acid on DNA synthesis in LLC cells, adherence of LLC cells to human adult dermal microvascular endothelial cells (HMVEC), and Matrigel-induced angiogenesis (in vitro and in vivo) were tested. Carp oil inhibited DNA synthesis in LLC cells at 100 and 1000 pg/mL, but not at 0.1 to 10 pg/mL Table (10) . Oleic acid inhibited DNA synthesis in LLC cells at 1000 pM Table (11) . Carp oil inhibited the Matrigel-induced tube-like network formation of HMVEC at 1000 pg/mL, but not at 0.1 to 100 pg/mL Table (10) . 

Table 11. Effects of oleic acid on DNA synthesis in LLC cells, Matrigel-induced capillary-like tube network Formation from HMVEC, and the adherence ofLLC cells to HMVEC (in vitro)1...

On the other hand, the inhibitory actions of oleic acid on metastasis in the liver and metastatic tumor growth in the liver, cannot be explained by the effects of DNA synthesis in LLC cells, and microvascular endothelial cells, or the adherence of LLC cells to the microvascular endothelium rather, these inhibitory actions by oleic acid are partly attributable to the inhibition of the angiogenesis induced by tumors. In conclusion, it seems likely that the antitumor and antimetastatic activities of carp oil may be partly ascribed to a fatty acid, oleic acid, as an active substance. However, the antitumor and antimetastatic effects of carp oil are insufficiently by themselves to explain the action of oleic acid. Further work is in progress to identify the active substance(s) in carp oil. 

In primary rahhit proximal tuhular (RPT) cells cisplatin exposure resulted in an inhihition of DNA synthesis, which is most likely related to the primary anti-tumorigenic mechanism of this compound i.e. DNA inter and intra strand cross linking [117]. RNA and protein synthesis were decreased in RPT cells and quiescent LLC-PK cells upon cisplatin exposure [117, 118]. Other effects of cisplatin on cultured RPT include a decrease in glucose uptake, an inhihition of Na -K ATPase and alterations in total glutathione content [117]. In the normal rat kidney (NRK) cell hne cisplatin (IpM for 48h) induced a marked increase in the level of lipid peroxides [119]. 

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