A model using semidomesticated mink was set up to study the effects of chronic oral methylmercury exposure in piscivorous mammals. Three groups of mink were fed daily with diets containing approximately 0.1, 0.5, and 0.9 micrograms/g of total mercury. Piscivorous and non-piscivorous fish, naturally contaminated with methylmercury, were used to prepare diets. Renal injury was evaluated using total urine protein/creatinine ratio and differentiation of urinary low-molecular-weight and high-molecular-weight proteins on sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The significance of the total urine protein/creatinine ratio data was assessed by comparing the results to a 95% group-based reference interval. The values for total urine protein/creatinine ratio did not reveal any significant increased excretion, and no dose-related trends were observed within the reference interval. Overall the total urine protein data did not suggest renal damage. Analysis of the SDS-PAGE electrophoretograms did not suggest the presence of any persistent glomerular damage in any group. High-molecular-weight proteins were not detected more frequently for any of the dose groups. During the adaptation phase, the B2M-like protein band was not remarked during the visual analysis of the gels. The B2M-like protein band was remarked during the gel analysis only several weeks into the exposure phase. This B2M-like protein band was more prevalent in urine samples taken from minks in the 0.5 and 0.9 micrograms/g groups than in the 0.1 microgram/group. These latter data, however, did not allow an evaluation of a quantitative dose-response excretion with time. The B2M-like data are suggestive of very minor renal injury.
After the Saint-basile-le-Grand region, Province of Quebec, Canada, was contaminated by PCBs, sixty-five beef cattle heifers were housed at an experimental farm for a period of ten months. Body fat PCB levels were measured on day 0, 117 and 203 of the study to determine if the beef cattle could eliminate these xenobiotics over a ten month period when fed an equilibrated ration. Clinico-pathological parameters and weight gain were measured at various intervals during this study to evaluate the long term health effects of PCBs on the heifers.On day 0 of the study, which is actually 160 days after the PCB fire, the highest PCB level found was 3.20 µg/g of body fat. The mean body fat PCB level was 0.52 µg/g at the start of the study. Congeners BZ #118, BZ #138, BZ #153 and BZ #180 represented approximately 80% of all the PCBs present in the body fat on day 0 of the study. The body fat PCB levels declined either by metabolism or dilution during the study since the body fat PCB levels decreased to a mean value of 0.09 µg/g on day 203.The only clinical test that suggested the presence of a reversible effect was the trend observed for the aspartate aminotransferase (AST) levels. The clinical data showed a decrease in the mean AST levels from 96 IU/L on day 0 to 70 IU/L on day 203 of the study. Throughout the study the AST levels were always within the reference range established for healthy cattle. Therefore, these results did not indicate the presence of a significant clinical effect. The observed AST trend only suggested that the PCB exposure may have caused this reversible effect. In coonclusion, the clinico-pathological data did not reveal the presence of a measurable long term health effect in the heifers.
Seven porphyrins previously suggested as biomarkers of chemical stress in mammals were identified and quantified in the freshwater mussels Elliptio complanata and Anodonta grandis grandis. Uroporphyrin, heptacarboxyporphyrin, hexacarboxyporphyrin, pentacarboxyporhyrin, coproporphyrin and protoporphyrin IX were determined using a method based on esterification of carboxylic acid moieties with BF3-methanol, extraction of the derivatives in chloroform, and HPLC–fluorescence analysis. Porphyrin profiles were compared in reference mussels sampled from nonpolluted lakes versus mussels exposed to 100 μg Cd/L in iron deficient conditions in the laboratory for 1 month or 54–177 ng Cd/L for 4–5 years in an experimental lake (northwestern Ontario, ELA, lake 382). The levels of protoporphyrin and mesoporphyrin were markedly elevated in specimens exposed to iron/salts deficiency and 100 μg Cd/L. In mussels sampled from lake 382, abnormal alterations in the relative proportions of uroporphyrin to heptacarboxyporphyrin, heptacarboxy- to meso-porphyrin, heptacarboxy- to proto-porphyrin, coproporphyrin to mesoporphyrin, and copro- to proto-porphyrin were consistent with a cadmium-mediated response. Thus, differences in the relative proportions of porphyrins, especially those associated with the accumulation of heptacarboxyporphyrin, indicate that Cd may be inhibiting uroporphyrinogen decarboxylase, suggesting potential applications of mussels' porphyrin profile as an ecotoxicological biomarker for Cd and possibly other metals.
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