Dietary supplementation of α-linolenic acid induced conversion of n-3 LCPUFAs and reduced prostate cancer growth in a mouse model.

Key Findings:

In a previous study, in which 0–10 wt% of ALA was added to the diet, it was demonstrated that mice effectively absorbed ALA as a dietary supplement.  Another study demonstrated that n-3 LCPUFAs inhibited prostate cancer growth and development in Pten-knockout mice, which develop prostate cancer spontaneously. In this study, prostate-specific Pten-knockout mice fed an ALA-enriched diet with defined PUFA levels was used to investigate the influence of dietary ALA on the level of n-3 LCPUFAs in vivo and its effect on tumour growth. Here ALA triggered significant increases in ALA, EPA, DPA and DHA levels and significant decreases in AA levels in blood, liver and prostate tissues compared with the control group when the mice were in the growth stage. A dose-dependent effect was observed for ALA and EPA and DPA, but not DHA. This is one of the first studies to demonstrate that dietary ALA can delay prostate tumour formation and progression as marine-derived oil. However, mice fed ALA diets exhibited significantly higher levels of plasma total cholesterol and LDL-cholesterol than the n-3 and EPA groups. In addition, the H-ALA diet produced a significant increase in serum alanine aminotransferase compared with controls. These results require further confirmation.

ABSTRACT

BACKGROUND: α-linolenic acid (ALA) is an n-3 polyunsaturated fatty acid (PUFA) and the substrate for long-chain n-3 PUFAs. The beneficial effects of ALA on chronic diseases are still in dispute, unlike those of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). METHODS: The primary objective of this investigation was to evaluate the efficiency of ALA uptake from a vegetable oil source and its subsequent conversion to n-3 long-chain PUFAs (LCPUFAs) in the tissues of growing mice, and to investigate its protective role in a prostate cancer animal model. We carried out the investigation in prostate-specific Pten-knockout mice with specified low-ALA (L-ALA, 2.5%) and high-ALA (H-ALA, 7.5%) diets. Total fatty acids in blood, liver, epididymal fat pad, prostate were detected and prostate weight were adjusted for body weight (mg/25 g). RESULTS: We found that dietary ALA triggered significant increases in ALA, EPA, docosapentaenoic acid (DPA) and DHA levels and a significant decrease in arachidonic acid levels during the mice’s growth stage. A dose-dependent effect was observed for ALA, EPA and DPA, but not DHA. Furthermore, the average prostate weights in the L-ALA and H-ALA groups were lower than those in the control and n-6 groups, and similar to those in the EPA and n-3 groups. CONCLUSIONS: Our data suggest that dietary supplementation with ALA is an efficient means of improving n-3 LCPUFAs in vivo, and it has a biologically effective role to play in prostate cancer, similar to that of fish oils.