AIM:To investigate the effect of retinoic acid (RA) on cellproliferation kinetics and retinoic acid receptor (RAR)expression of colorectal mucosa.METHODS:One hundred sixty healthy male Wistar ratswere randomly divided into 4 groups.Rats in groups I andII were subcutaneously injected with dimethylhydrazine(DMH) (20 mg/kg,once a week,) for 7 to 13 weeks,whilegroups Ⅲ and Ⅳ were injected with normal saline.Rats ingroups Ⅱ and Ⅲ were also treated with RA (50 mg/kg,every day,orally) from 7th to 15th week,thus group Ⅳ wasused as a control.The rats were killed in different batches.The expressions of proliferating cell nuclear antigen (PCNA),nucleolar organizer region-associated protein (AgNOR) andRAR were detected.RESULTS:The incidence of colorectal carcinoma wasdifferent between groups Ⅰ (100 %) and Ⅱ (15 %) (P<0.01).The PCNA indices and mean AgNOR count in group Ⅱ weresignificantly lower than those in group Ⅰ(F=5.418 and 4.243,P<0.01).The PCNA indices and mean AgNOR count in groupsⅠ and Ⅱ were significantly higher than those in the groupsⅢ and Ⅳ (in which carcinogen was not used) (F=5.927and 4.348,P<0.01).There was a tendency in group Ⅰ thatthe longer the induction with DMH the higher PCNA indexand AgNOR count expressed (F=7.634 and 6.826,P<0.05).However,there was no such tendency in groups Ⅱ,Ⅲ andⅣ (F=1.662 and 1.984,P>0.05).The levels of RAR in normaland cancerous tissues in groups treated with RA weresignificantly higher than those in groups not treated withRA (F=6.343 and 6.024,P<0.05).CONCLUSION: RA decreases the incidence of colorectal carcinoma induced by DMH. Colorectal cancer tissue is associated with abnormal expression of PCNA, AgNOR and RAR. RA inhibits the expression of PCNA and AgNOR, and increases RAR concentration in colorectal tissues. AIM: To investigate the effect of retinoic acid (RA) on cellproliferation kinetics and retinoic acid receptor (RAR) expression of colorectal mucosa. METHODS: One hundred sixty healthy male Wistar ratswere randomly divided into 4 groups. Rats in groups I and II were subcutaneously injected with dimethylhydrazine (DMH) (20 mg / kg, once a week,) for 7 to 13 weeks, whilegroups III and IV were injected with normal saline. Rats ingroups II and III were also treated with RA (50 mg / kg, every day , orally) from 7th to 15th week, thus group IV wasused as a control. These rats were killed in different batches. The expressions of proliferating cell nuclear antigen (PCNA), nucleolar organizer region-associated protein (AgNOR) andRAR were detected .RESULTS The incidence of colorectal carcinoma wasdifferent between groups I (100%) and II (15%) (P <0.01). PCNA indices and mean AgNOR count in group II weresignificantly lower than those in group I (F = 5.418 and 4.243, P <0.01). PCNA indices and mean AgNOR count in groups I and II were significantly higher than those in the groups III and IV (in which carcinogen was not used) (F = 5.927 and 4.348, P <0.01) .There was a tendency in group I that the longer the induction with DMH the higher PCNA There was no such tendency in groups Ⅱ, Ⅲ and Ⅳ (F = 1.662 and 1.984, P> 0.05). The levels of RAR in normaland cancerous tissues in groups treated with RA weresignificantly higher than those in groups not treated with RA (F = 6.343 and 6.024, P <0.05) .CONCLUSION: RA decreases the incidence of colorectal carcinoma induced by DMH. Colorectal cancer tissue is associated with abnormal expression of PCNA, AgNOR and RAR. RA inhibits the expression of PCNA and AgNOR, and increases RAR concentration in colorectal tissues.