In this study, cadmium (Cd) accumulation was studied in an experimental aquatic exposure. Mosquitofish (Gambusia affinis) were acutely exposed for 96 h to a high concentration of Cd (12 mg/L) and were chronically exposed to a low concentration of Cd(0.4 mg/L) for 30 days. Cd accumulation profiles differed between the two Cd exposures. The Cd concentation in G. affinis tissues increased linearly during acute exposure. In contrast, chronic exposure presented a biphasic pattern of accumulation, with Cd accumulation increasing until 20 days post-exposure then decreasing by the 30th day of the experiment. Histopathological investigations revealed greater changes in gills, kidney and liver tissues after chronic exposure than those recorded during acute exposure. The changes in gill were characterized by epithelial lifting, total and partial lamellar fusion, epithelial necrosis as well as telangiectasis. Necrosis of epithelial cells of renal tubules, glomerular contraction and reduction of Bowman’s space were observed in the kidney tissue of exposed fish. The liver hepatocytes showed cytoplasmic vacuolization with lipid droplets and glycogen accumulation. Desquamation of hepatic tissue, congestion of the hepatic central vein and an increase in sinusoidal space were also observed. The result showed that, although Cd accumulation, following acute and chronic exposure, severely affects vital organs in mosquitofish; G. affinis adapts to continued metal accumulation. We hypothesise that this adaptation occurs through activation of a metal resistance mechanism.