No abstract

From the point of view of human exposure, fumonisins (FB1, FB2, FB1, FB4), a relatively recently (1988) discovered and identified group of mycotoxins, represent one of the five most important mycotoxin groups causing human disease. In an earlier experiment studying the effects of relatively low doses (10, 20 and 40 p.p.m.) of FB1 in weaned piglets, it was established that the 4-week feeding of 10 p.p.m. (mg/kg feed) FB1 produced mild pulmonary oedema. This suggested the importance of studies with even lower doses of the toxin to determine the tolerable limits. The objective of this experiment was therefore to study the effects of prolonged (8-week) exposure to still lower concentrations (0, 1, 5 and 10 mg/kg feed) of FB1. The 8-week feeding of FB1 in low concentrations (1-10 p.p.m.) did not cause clinical signs and significant performance impairment in pigs, but rendered irreversible the chronic changes that had already developed in the animals in a dose-dependent manner. Dissection revealed pathological alterations of the lungs in one of the animals given 1 p.p.m. (n = 4), in two animals exposed to 5 p.p.m. (n = 5), and in three animals given 10 p.p.m. (n = 4). In all three treatment groups, proliferation of the connective tissue fibres, primarily of those around the lymphatic vessels, in the subpleural and interlobular connective tissue of the lungs, extending to the peribronchial and peribronchiolar areas, was seen. The results of this experiment call attention to the risk of prolonged low-dose toxin exposure, which has very important public health implications.

Ochratoxin A (OTA) is a nephrotoxic and carcinogenic mycotoxin, a secondary metabolite produced by mould fungi belonging to several Aspergillus and Penicillium species. It is formed during the storage of cereal grains and other plant-derived products. OTA ingested by humans and animals with the food or feed may exert deleterious effects on health. The purpose of this study was to investigate the ochratoxin contamination of the most important potential sources of OTA. The OTA content of cereal samples for human consumption (36 baking wheat, 16 wheat flour and 6 maize coarse meal samples) and feed grain samples (30 feeding wheat, 32 feeding maize and 20 feeding barley samples) collected in the mid-phase or at the end of the storage period and of 50 commercial coffee samples was determined. The analyses were performed by immunoaffinity column -high-performance liquid chromatography (IAC-HPLC). The limit of detection of the method was 0.1 ng/g. Of the wheat samples intended for human consumption, 8.3% contained OTA at 0.29 ng/g on the average (OTA ranges: 0.12-0.5 ng/g; Table 2). The OTA contamination of wheat flour and maize meal samples for human consumption was similar to that of the baking wheat samples. OTA contamination was found in 26.7% of the feeding wheat, 15.6% of the feeding maize and 35% of the feeding barley samples. The average values and the ranges of OTA levels found in the above samples were 12.2 and 0.3-62.8 ng/g, 4.9 and 1.9-8.3 ng/g, and 72 and 0.14-212 ng/g, respectively (Table 3). Sixty-six percent of the coffee samples were contaminated with OA (average level: 0.57 ng/g, ranges: 0.17-1.3 ng/g; Table 4). OTA contamination of baking wheat samples was found to be relatively low, presumably as a result of the favourable weather at harvest and the optimal storage conditions. Calculations made on the basis of the obtained results show that the daily OTA intake of an adult human from edible cereals is only 6.7 ng, while the amount taken up with coffee is 4.1 ng daily. The high prevalence and high levels of OTA contamination in feed grains can be explained by the unfavourable storage conditions, and this finding suggests that OA-related health problems may arise in animals, and that foods of animal origin may be contaminated with this mycotoxin.

The effect of synthetic beta-carotene and synthetic nucleotide base on daily weight gain, feed consumption and certain haematological, biochemical and immunological parameters of piglets were studied in a 3-week experiment. Beginning one week prior to weaning, the diet fed to one experimental group of piglets was supplemented with 10% Rovimix Beta-carotene at 875 mg/kg of diet. Synthetic uracil and adenine (98%, Sigma-Aldrich) were mixed into the diet of the other experimental group at doses of 500 mg/kg of diet for each substance. The control group received the basic diet without any supplementation. The changes observed over time in the haematological parameters and in certain biochemical variables could be regarded as physiological. By day 21 of the experiment, beta-carotene supplementation had significantly lowered the neutrophilic granulocyte percentage and elevated the lymphocyte percentage, while in the other two groups a change of opposite tendency occurred. At the end of the experimental period there was a decrease in plasma vitamin E concentration due to carotene supplementation (control: 6.1 ± 1.5, nucleotide: 6.3 ± 2.5, carotene: 2.3 ± 1.5 mg/L). Lymphocyte blastogenesis induced by phytohaemagglutinin and concanavalin A increased by 50 and 130%, respectively, in the nucleotide group and by 60 and 30%, respectively, in the carotene group, while it did not change in the control group. The supplements exerted no positive effect on the in vivo cellular immune response.

Three sows were fed a diet mixed with Fusarium moniliforme fungal culture from the 107th day of pregnancy until parturition. Fumonisin B(1) toxin was administered to two sows (sows 1 and 2) in a daily dose of 300 mg for an additional 7 days subsequent to parturition, i.e., for a total of 14-16 days. The third sow (No. 3) was given the toxin in the same daily dose only until parturition, i.e., for 7 days in total. There were no symptoms observed in any of the sows. Two piglets were taken from each of the three sows and sacrificed immediately after parturition, i.e., prior to the first suckling. After 24 h, two additional piglets were taken for slaughter from each of the litters, which by then had access to colostrum. Finally, on the 7th day postparturition another two piglets per litter were sacrificed and material obtained from them was processed for examination. It was established that fumonisin B(1) present in the Fusarium moniliforme culture resulted in damage to the fetuses in utero. Of the changes indicating toxic effect, intraalveolar, subpleural, and interstitial pulmonary edema of various degrees of severity could be detected in the piglets sacrificed immediately following parturition and before the first suckling. Pathological changes were observed in the histopathological sections of the liver, and increases in the activities of plasma aspartic acid transaminase (AST), gamma glutamyl transferase (GGT) and alkaline phosphatase (AKLP), higher than physiological levels were detected. The serum-free sphinganine/sphingosine ratio, considered a bioindicator of fumonisin B(1) toxicosis, varied in accordance with the degree of severity of the changes which occurred. The values obtained were found to be between 0.29 and 0.36 in the cases of severe pulmonary edema, and between 0.20 and 0.24 for the cases of mild pulmonary edema. In the piglets of the sows fed the toxin for an additional 7 days subsequent to parturition and which were born with severe pulmonary edema, mild pulmonary edema could be detected after colostrum suckling, 24 h, and 7 days after parturition. The SA/SO value of the serum in these two piglets was 0.19 and 0.20, while at the same time AST, GGT, and ALKP values higher than physiological levels were measured. In the milk samples taken from sows 1 and 2 and examined after 24 h and after 7 days FB(1) was detected in quantities of 18.0-27.5 ppb. There were no changes observed on the seventh day in the piglets of the third sow, the diet of which contained no toxin after parturition. However, as the piglets of the third sow demonstrated only mild effects of pulmonary edema it is not possible to establish with certainty a postpartum cause-effect relationship between fumonisin in colostrum and pulmonary edema.