Proceedings of The Physiological Society

Future Physiology (Leeds, UK) (2017) Proc Physiol Soc 39, PC03

Poster Communications

Cadmium exacerbates acetic acid induced experimental colitis in rats

A. G. Adegoke1, A. T. Salami1, S. B. Olaleye1

1. Physiology, University of Ibadan, Ibadan, Nigeria.

Increase in the incidences of inflammatory bowel disease in developing countries is a pointer to the role metal toxicants may play in its pathogenesis; cadmium 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 induced colitis in rats. Wistar rats (male, 100-120 g, n=5) 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. Rats were anaesthetised with ketamine (35 mg kg-1, i.p.) and thereafter, induced with colitis by intra-rectal administration of 2 mL 4% acetic acid (Morris et al., 1989). Weekly body weight, daily diarrheal scores, macroscopic scores and organ weights were recorded, blood was collected from each rat and colons were resected after an overdose of anaesthesia at each of days 0, 3, 7 and 14 of colitis induction. Neutrophil/lymphocyte ratio (NLR) was determined, blood cadmium and malondialdehyde (MDA) concentrations were assessed by spectrophotometry. Regeneration in colonic tissues were studied microscopically. Values are means ± S.E.M., compared by ANOVA. Blood cadmium concentration (ppm) was high in Cd50 (0.04±0.00) and Cd100 (0.04±0.00) vs. control (0.03±0.00), p<0.05. Cadmium decreased weight gain (%) at weeks 3 and 4 in Cd100 (128.07±3.40; 123.57±3.34) vs. control (141.75±4.75; 139.65±4.51), p<0.05. Cadmium increased; stool consistency scores at day 5 in Cd100 (2.50±0.22) vs. control (1.50±0.22), p<0.05, neutrophil/lymphocyte ratio at days 0 and 7 in Cd50 (0.43±0.04; 0.80±0.06) and Cd100 (0.49±0.03; 0.80±0.03) vs. control (0.36±0.03; 0.63±0.04), p<0.05 and colonic MDA concentration (nmol mg/protein) in each of Cd25, Cd50 and Cd100 at day 7 (0.56±0.02; 0.61±0.03; 0.65±0.01) vs. control (0.50±0.02), p<0.05 and at day 14 (0.41±0.02; 0.52±0.02; 0.60±0.02) vs. control (0.31±0.00), p<0.05. Colon histopathology persisted till day 14 in Cd100. These data suggest that sub-chronic oral exposures to cadmium delayed the healing of acetic acid induced colitis and inflammatory pathways may be implicated.

Where applicable, experiments conform with Society ethical requirements