PURPOSE: The present study was conducted to elucidate the potential of selenium supplementation, if any, in affording chemoprevention by modulating the altered cancer markers and ultrastructural changes in dimethyl hydrazine (DMH)-induced colorectal carcinogenesis in rats. METHODS: The rats were segregated into four groups, viz., normal control, DMH treated, selenium treated, and DMH + selenium treated. Initiation and induction of colon carcinogenesis was achieved through weekly subcutaneous injections of DMH (30 mg/kg body weight) for both 10 and 20 weeks. Selenium was supplemented to rats at a dose level of 1 ppm in drinking water ad libitum for two different time durations of 10 and 20 weeks. RESULTS: The study observed a significant increase in the number of aberrant crypt foci (ACF) in colons of DMH-treated rats at both time intervals which were decreased significantly upon selenium supplementation. Also, a significant increase was seen in the enzyme activity of alkaline phosphatase (ALP), which, however, was moderated upon selenium administration to DMH-treated rats. Changes in the ultrastructural architecture of colonic cells were apparent following both the treatment schedules of DMH; however, the changes were prominent following 20 weeks of DMH treatment. The most obvious changes were seen in the form of altered nuclear shape and disruption of cellular integrity, which, upon selenium supplementation, were appreciably improved. CONCLUSION: In conclusion, the study shows the chemopreventive abilities of selenium against DMH-induced colorectal carcinogenesis in rats.
PURPOSE: The present study was conducted to elucidate the potential of selenium supplementation, if any, in affording chemoprevention by modulating the altered cancer markers and ultrastructural changes in dimethyl hydrazine (DMH)-induced colorectal carcinogenesis in rats. METHODS: The rats were segregated into four groups, viz., normal control, DMH treated, selenium treated, and DMH + selenium treated. Initiation and induction of colon carcinogenesis was achieved through weekly subcutaneous injections of DMH (30 mg/kg body weight) for both 10 and 20 weeks. Selenium was supplemented to rats at a dose level of 1 ppm in drinking water ad libitum for two different time durations of 10 and 20 weeks. RESULTS: The study observed a significant increase in the number of aberrant crypt foci (ACF) in colons of DMH-treated rats at both time intervals which were decreased significantly upon selenium supplementation. Also, a significant increase was seen in the enzyme activity of alkaline phosphatase (ALP), which, however, was moderated upon selenium administration to DMH-treated rats. Changes in the ultrastructural architecture of colonic cells were apparent following both the treatment schedules of DMH; however, the changes were prominent following 20 weeks of DMH treatment. The most obvious changes were seen in the form of altered nuclear shape and disruption of cellular integrity, which, upon selenium supplementation, were appreciably improved. CONCLUSION: In conclusion, the study shows the chemopreventive abilities of selenium against DMH-induced colorectal carcinogenesis in rats.
Authors: K W Kinzler; M C Nilbert; B Vogelstein; T M Bryan; D B Levy; K J Smith; A C Preisinger; S R Hamilton; P Hedge; A Markham Journal: Science Date: 1991-03-15 Impact factor: 47.728