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Abstract

Liver lipid changes in male BALB-c nude mice due to subcutaneously implanted human prostate metastatic grade IV adenocarcinoma was studied. The prostate cancer cells were cultured in F12 plus 7.5% horse serum and 25% fetal calf serum medium. When they reached confluence, some of these cells were fixed with glutaraldehyde and thoroughly washed with buffer then 4 x107 cells were implanted into four mice. Four more mice were implanted with 4 x 106 viable, unfixed cells. Four uninjected mice served as controls. All the mice were sacrificed 18 days later. The total liver lipids (TLL) from each liver were extracted with chloroform: methanol and dried in separate vials under a stream of gaseous nitrogen. While being dried, the TLL of each liver sample were weighed intermittently until their weight remained constant. The weight of TLL in each vial was then divided by the wet weight of each corresponding extracted liver. This was done to normalize the liver lipids in terms of one gram of liver because livers of different wet weights were extracted. The TLL per gram of wet liver were similar in the control and livers of mice injected with viable cancerous cells and decreased in the livers of mice injected with glutaraldehyde-fixed cells. When the total lipids were fractionated into polar and nonpolar lipids on silicic gels, entirely different changes were seen. The TLL of the mice injected with untreated viable cancer cells and those injected with glutaraldehyde-fixed cells were similar while the control liver lipids classes were significantly different. There was a decrease in the percentage of neutral lipids and an increase in the polar fractions in the two groups of mice injected with either cells. The growth of the viable injected prostate cells did not cause any unique lipid changes in these two lipid class profiles. However, the triglycerides and total cholesterol showed wide variations among the livers of mice injected with viable cancer cells. The ratio of the polar/neutral lipids did not differ between the mice injected with either cells. Thus, the present study does not support the accepted explanation that the rapidly growing cancer cells are mainly responsible for the lipid changes seen in animals implanted with other types of tumor cells.

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