Inhibition of conjugated linoleic acid on mouse forestomach neoplasia induced by benzo (a) pyrene and chemopreventive mechanisms

AIM: To explore the inhibition of conjugated linoleic acid isomers in different purity (75 % purity c9,t11-, 98 % purity c9,t11- and 98 % purity t10,c12-CLA) on the formation of forestomach neoplasm and cheopreventive mechanisms. METHODS: Forestomach neoplasm model induced by B(a) P in KunMing mice was established. The numbers of tumor and diameter of each tumor in forestomach were counted; the mice plasma malondialdehyde (MDA) were measured by TBARS assay; TUNEL assay was used to analyze the apoptosis in forestomach neoplasia and the expression of MEK-1, ERK-1, MKP-1 protein in forestomach neoplasm were studied by Western Blotting assay. RESULTS: The incidence of neoplasm in B(a)P group, 75 % purity c9, t11-CLA group, 98 % purity c9,t11-CLA group and 98 % purity t10, c12-CLA group was 100 %, 75.0 % (P>0.05), 69.2 % (P<0.05) and 53.8 % (P<0.05) respectively and the effect of two CLA isomers in 98 % purity on forestomach neoplasia was significant; CLA showed no influence on the average tumor numbers in tumor-bearing mouse, but significantly decreased the tumor size, the tumor average diameter of mice in 75 % purity c9,t11-CLA group, 98 % purity c9,t11-CLA group and 98 % purity t10, c12-CLA group was 0.157+/-0.047 cm, 0.127+/-0.038 cm and 0.128+/-0.077 cm (P<0.05) and 0.216+/-0.088 cm in B(a)P group; CLA could also significantly increase the apoptosis cell numbers by 144.00+/-20.31, 153.75+/-23.25, 157.25+/-15.95 (P<0.05) in 75 % purity c9,t11-CLA group, 98 % purity c9, t11-CLA group and 98 % purity t10,c12-CLA group (30.88+/-3.72 in BP group); but there were no significant differences between the effects of 75 % purity c9,t11-CLA and two isomers in 98 % purity on tumor size and apoptotic cell numbers; the plasma levels of MDA in were increased by 75 % purity c9,t11-CLA, 98 % purity c9,t11-CLA and 98 % purity t10,c12-CLA. The 75 % purity c9,t11-CLA showed stronger inhibition; CLA could also inhibit the expression of ERK-1 protein and promote the expression of MKP-1 protein, however no influence of CLA on MEK-1 protein was observed. CONCLUSION: Two isomers in 98 % purity show stronger inhibition on carcinogenesis. However, the inhibitory mechanisms of CLA on carcinogenesis is complicated, which may be due to the increased mice plasma MDA, the inducing apoptosis in tumor tissues. And the effect of CLA on the expression of ERK-1 and MKP-1 may be one of the mechanisms of the inhibition of CLA on the tumor.