{"title":"Cadmium Exacerbates Acetic Acid Induced Experimental Colitis in Rats","authors":"Adegoke Ag, A. Salami, S. Olaleye","doi":"10.21767/2248-9215.100027","DOIUrl":null,"url":null,"abstract":"Background: Increase in the incidences of inflammatory bowel disease (IBD) in developing countries is a pointer to the role metal toxicants may play in its pathogenesis. Cadmium (Cd) has been implicated in the etiology of diseases involving several tissues including the colonic mucosa. This present study aimed at investigating the effects of oral cadmium exposures on healing of acetic acid (AA)-induced colitis in rats. Methods and Findings: Male Wistar rats (100-120 g) were grouped and exposed to cadmium as follows: Control (water), Cd25 (25 ppm CdCl2), Cd50 (50 ppm CdCl2), Cd100 (100 ppm CdCl2) for four weeks. Colitis was induced by intrarectal administration of 2 ml 4% acetic acid. Rats were sacrificed and colons were resected on days 0, 3, 7 and 14 of colitis induction. Weekly body weight, diarrheal and macroscopic scores, organ weights, neutrophil/lymphocyte ratio (NLR), malondialdehyde (MDA) concentration, and regeneration in colonic tissues were studied microscopically. Cadmium significantly (p<0.05) decreased weight gain (%) at weeks 3 and 4 in Cd100 group, significantly (p<0.05) increased stool consistency scores on day 5 in Cd100 group, increased colon macroscopic scores in Cd100 group on days 3 and 7, significantly (p<0.05) increased neutrophil/ lymphocyte ratio on days 0 and 7 in Cd50 and Cd100, and colonic MDA concentrations in each of Cd25, Cd50 and Cd100 from day 3 till day 14. Colon histopathology persisted till day 14 in Cd100 group. Conclusions: These data indicate that cadmium delayed healing of acetic acid induced colitis and inflammatory pathways may be implicated.","PeriodicalId":12012,"journal":{"name":"European Journal of Experimental Biology","volume":"8 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Experimental Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21767/2248-9215.100027","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5
Abstract
Background: Increase in the incidences of inflammatory bowel disease (IBD) in developing countries is a pointer to the role metal toxicants may play in its pathogenesis. Cadmium (Cd) has been implicated in the etiology of diseases involving several tissues including the colonic mucosa. This present study aimed at investigating the effects of oral cadmium exposures on healing of acetic acid (AA)-induced colitis in rats. Methods and Findings: Male Wistar rats (100-120 g) were grouped and exposed to cadmium as follows: Control (water), Cd25 (25 ppm CdCl2), Cd50 (50 ppm CdCl2), Cd100 (100 ppm CdCl2) for four weeks. Colitis was induced by intrarectal administration of 2 ml 4% acetic acid. Rats were sacrificed and colons were resected on days 0, 3, 7 and 14 of colitis induction. Weekly body weight, diarrheal and macroscopic scores, organ weights, neutrophil/lymphocyte ratio (NLR), malondialdehyde (MDA) concentration, and regeneration in colonic tissues were studied microscopically. Cadmium significantly (p<0.05) decreased weight gain (%) at weeks 3 and 4 in Cd100 group, significantly (p<0.05) increased stool consistency scores on day 5 in Cd100 group, increased colon macroscopic scores in Cd100 group on days 3 and 7, significantly (p<0.05) increased neutrophil/ lymphocyte ratio on days 0 and 7 in Cd50 and Cd100, and colonic MDA concentrations in each of Cd25, Cd50 and Cd100 from day 3 till day 14. Colon histopathology persisted till day 14 in Cd100 group. Conclusions: These data indicate that cadmium delayed healing of acetic acid induced colitis and inflammatory pathways may be implicated.