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Lithocholic acid (LCA) is implicated in human and experimental animal carcinogenesis. Its effect on apoptosis and proliferation of the colonic epithelium was studied in a 1,2-dimethylhydrazine (DMH)-induced murine carcinogenesis model. Four groups of mice, control, LCA, DMH and DMH+LCA, were studied for 4 weeks, a period corresponding to early stages of carcinogenesis. Apoptosis (AI) and proliferation (PI) indices in the colon were determined by immunohistochemistry. LCA stimulated apoptosis (AI = 1.2 ± 0.3% (all values are the mean ± SEM) versus control 0.5 ± 0.1%, P < 0.05), as did DMH (4.3 ± 0.8%, P < 0.02). DMH increased apoptosis at the base of the crypt nearly 50-fold, with no effect at the lumenal third. In mice receiving DMH, LCA suppressed apoptosis almost completely (0.1 ± 0.03%); this suppression was complete at the lower two-thirds of the crypt (AI = 0) and 60% at the lumenal third. LCA increased proliferation (PI = 22.2 ± 4.6% versus 15.4 ± 1% in controls), but this did not reach statistical significance. DMH increased proliferation (PI = 34.6 ± 2.3%, P < 0.01). In mice receiving DMH, proliferation (41 ± 2.9%) was about two-thirds of the additive effect. LCA affected proliferation, mainly in the middle third of the crypt; DMH's effect was similar in distribution, but more pronounced. In mice receiving DMH, LCA shifts proliferation upward, extending it to the lumenal third of the crypt. LCA's main cell kinetic effect in the colon is on apoptosis; this effect differs in normal (stimulation) and pre-malignant colon (nearly complete suppression). LCA does not significantly stimulate proliferation in either normal or pre-malignant colon. The differential effect of LCA on apoptosis in the presence of a carcinogen partially explains its effect as a promoter on colon carcinogenesis in animal models, and may have important implications for human carcinogenesis. Key words AI, apoptosis index DMH, 1,2-dimethylhydrazine LCA, lithocholic acid PCNA, proliferating cell nuclear antigen PI, proliferation index RT, room temperature TUNEL, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling. © Oxford University Press « Previous | Next Article » Table of Contents This Article Carcinogenesis (2000) 21 (5): 999-1005. doi: 10.1093/carcin/21.5.999 » Abstract Free Full Text (HTML) Free Full Text (PDF) Free Classifications Carcinogenesis Services Article metrics Alert me when cited Alert me if corrected Find similar articles Similar articles in Web of Science Similar articles in PubMed Add to my archive Download citation Request Permissions Citing Articles Load citing article information Citing articles via CrossRef Citing articles via Scopus Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Kozoni, V. Articles by Rigas, B. 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Carcinogenesis – Oxford University Press
Published: May 1, 2000
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