论文部分内容阅读
AIM:To investigate the effect of ethylene diamine tetraaceticacid (EDTA) on proliferation of rat colonic cells.METHODS:EDTA was administered into Wistar rats,carcinogenesis induced by 1,2-dimethylhydrazine (DMH) inrats was studied with immunohistochemistry.RESULTS:Marked regional differences in cell proliferationwere found in all groups.In EDTA-treated animals,totallabelling indexes in both proximal (10.00±0.44 vs 7.20±0.45)and distal (11.05±0.45 vs 8.65±0.34) colon and proliferativezone size (21.67±1.13 vs 16.75±1.45,27.73±1.46 vs21.74±1.07) were significantly higher than that in normalcontrols (P<0.05) and lower than that in DMH group(10.00±0.44 vs 11.54±0.45,11.05±0.45 vs 13.13±0.46,21.67±1.13 vs 35.52±1.58,27.73±1.46 vs 39.61±1.32,P<0.05).Cumulative frequency distributions showed a shiftof the EDTA distal curve to the right (P<0.05) while theEDTA proximal curve did not change compared to normalcontrols.Despite the changes of proliferative parameters,tumours did not develop in EDTA treated animals.CONCLUSION:Hyperproliferation appears to be more easilyinduced by EDTA in distal colon than in proximal colon.Hyperproliferation may need to exceed a threshold to developcolonic turnouts.EDTA may work as a co-factor in colonictumorigenesis.
AIM: To investigate the effect of ethylene diamine tetraacetic acid (EDTA) on proliferation of rat colonic cells. METHODS: EDTA was administered into Wistar rats, carcinogenesis induced by 1,2-dimethylhydrazine (DMH) inrats was studied with immunohistochemistry .RESULTS: Marked regional differences in cell proliferationwere found in all groups.In EDTA-treated animals, total pregnancy indices in both proximal and proximal tubules (10.00 ± 0.44 vs 7.20 ± 0.45 and 6.4 ± 0.45 vs 8.65 ± 0.34, respectively) ± 1.45, 27.73 ± 1.46 vs. 21.74 ± 1.07) were significantly higher than that in normal controls (P <0.05) and lower than that in DMH group (10.00 ± 0.44 vs 11.54 ± 0.45, 11.05 ± 0.45 vs 13.13 ± 0.46, 21.67 ± 1.13 vs 35.52 ± 1.58,27.73 ± 1.46 vs 39.61 ± 1.32, P <0.05) .Cumulative frequency distributions showed a shift of the EDTA distal curve to the right (P <0.05) while theEDTA proximal curve did not change compared to normal controls .Despite the changes of proliferative parameters, tumours did not develop in EDTA treated animals.CONCLUSION: Hyperproliferation appears to be more easily induced by EDTA in distal colon than in proximal colon. Hyperproliferation may need to exceed a threshold to developcolonic turnout. EDTA may work as a co-factor in colonictumorigenesis.