A study was performed to determine aflatoxin residues in tissues and organs of male broilers and hens that had been fed a diet contaminated with 50 micrograms/kg aflatoxin B1 (AFB1). Residue levels of AFB1, aflatoxicol (Ro), aflatoxin M1 (AFM1) and aflatoxin B2a (AFB2a) were determined by an HPLC method and, with the exception of AFB2a, were detected in the liver, kidney and thigh of both male broilers and hens. The highest levels found were for Ro in liver (1.10 and 0.60 micrograms/kg for male broilers and hens, respectively). On the other hand no detectable amounts of aflatoxins were found in any tissue after withdrawal periods of 14 and 33 days for male broilers and laying hens respectively.
Studies were performed on the efficacy, residues and in vitro enterocyte toxicity of 4-hexylresorcinol (4-HR), which could be utilized as an inhibitor of shrimp melanosis (black spot). Mediterranean sea shrimp (Parapaeneus longirostris) were treated with solutions of 4-HR in sea-water, at three different concentrations, 25, 50 or 100 mg/kg of shrimp, to test its antioxidative property. As a comparison a group of shrimp was treated with sodium metabisulphite (1 g/kg), while another group was left untreated. 4-HR showed a marked ability to inhibit or slow down melanosis (black spot) in shrimp; the most effective concentration was 100 mg/kg within an optimum period of 7 days but with effects up to the tenth day. During the first 5 days, 4-HR residues in the edible part of the shrimp showed a fast decrease in all three groups, going from initial average values of 20 mg/kg at 0 time, to 0.9 in the group treated at 25 mg/kg; from 42 to 1.8 mg/kg in the group at 50 mg/kg and from 85 to 1.9 mg/kg in the group at 100 mg/kg. In vitro studies on enterocyte-like Caco-2 cells did not indicate any cytotoxic effect up to a concentration of 50 micrograms/ml. Moreover, no inhibition of protein synthesis was observed, which lends further support to the absence of significant damage to the intestinal mucosa induced by 4-HR. The available database on 4-HR pharmacology and toxicology is inadequate to determine even a provisional ADI. There is negative evidence of carcinogenesis and no significant untoward effects were observed in humans when it was used as an anthelmintic. However, it is not possible to determine a NOEL for non-genotoxic effects. 4-HR could become an interesting alternative to the use of sulphites to prevent black spot. However, a more complete database is needed to achieve a regulatory evaluation.
Algal extracts of Anabaena planctonica from Lake Mulargia in Italy were tested for toxins by mouse bioassay, the Microtox system, and GC-MS and HPLC chromatography. Anatoxin-a was identified by GC-MS after derivatization with pentafluorobenzyl bromide. Hepatotoxins were also present and are perhaps related to the microcystins present in other species of Anabaena.
The aim was to establish whether or not the repartitioning effect of the β-agonist clenbuterol is present on low food availability stressed broiler chickens. The authors were also interested in pathological events caused by the combination of severe underfeeding and clenbuterol administration
In January and September of 1989 and March 1990 blooms of Oscillatoria rubescens, Oscillatoria tenuis and Oscillatoria mougetii were found in Lake Simbirizzi and Lake Flumendosa in Sardinia, and in Lake San Puoto in the Lazio region of Italy. By using different extraction methods and HPLC analysis, two microcystin-like toxins (RR-like and YR-like), similar to some of the toxic compounds produced by the Cyanophycea Microcystis aeruginosa, were detected in these blooms.
A "red tide" bloom of Gonyaulax polyedra occurred in Italy in Autumn, 1988. Algal concentrated extracts and undiluted water samples from the bloom were tested both with the Microtox system and a mouse bioassay, revealing the presence of paralytic shellfish poison-like neurotoxins. Saxitoxin levels evaluated on the basis of toxicological and instrumental analysis showed discrepancies. Other toxins could be present in addition to paralytic shellfish poison.
An animal experiment was performed to evaluate the absorption and distribution of aluminium in serum and tissues of normal rats. The animals were intraperitoneally injected with an aluminium lactate solution at a pH adjusted to 7.0. Before starting, a short preliminary study was carried out in order to verify the validity of the treatment with aluminium lactate instead of aluminium chloride at endogenous pH 3.4. Thirty-one rats were used in the main experiment, divided in four groups. In treated animals, the total Al-administered dose was 75.6 mg during 78 days of treatment. Furthermore, to evaluate the influence of the parathyroid hormone on Al absorption and/or distribution, 200 USP/rat of parathyroid hormone extract (PTH) were also administered during the last 5 days of the experiment. Aluminium content in serum, tibia, rib, brain, liver, muscle, kidney and spleen was determined. Calcium analysis in serum and bone was also performed. The highest concentrations of aluminium were found in liver and spleen, whereas the lowest level was found in the brain. The PTH effect on Al absorption was evident in brain and bone.
In order to study the effect of aluminum intoxication on bone and bone cells in normal animals and its relationship with hyperparathyroidism, and so to obtain further data on a pathogenetic role of this condition in inducing osteomalacia in uremic patients, 31 rats divided in four groups were injected intraperitoneally for 11 weeks with: Al (75.6 mg); Al-PTH (Al = 75.6 mg + PTH = 200 USP during the last week); C (saline solution), and C-PTH (saline solution + PTH = 200 USP during the last week). Al injection induced a consistent increase in the element in serum and tibia. PTH administration further enhanced Al content in tibia. The trabecular bone surfaces of Al-administered rats were stained by aluminon; the endosteal borders of their compact bone were always negative. Rib histomorphometry showed absence of osteomalacia in Al group and increase in osteoid in Al-PTH group, with development of mild osteomalacia. In these groups osteoclasts were less numerous than in controls. Dynamic bone parameters showed no separation of double tetracycline labels in trabecular bone of both Al-administered groups. Cortical bone was only slightly affected by treatment. All these data indicate that Al alone, in the quantity administered, does not induce osteomalacia in normal rats and that PTH, although given for a few days, enhances Al content in bone and induces osteoid increment. The reduction of tetracycline labels in all Al-treated animals is due to reduction of calcification and formation rate, which might be an index of osteoblast inhibition. The decrease in the number of osteoclasts suggests that Al might inhibit their formation.
Aluminum concentrations were measured in serum and in the bone, liver, spleen, kidney and brain of male Wistar rats treated with aluminum lactate. The administration was performed intraperitoneally over a period of 109 days, giving a total elemental aluminum dose of 128 mg per rat. After loading, a group of animals was killed together with blanks to verify the level of aluminum accumulation. Two groups of remaining rats were administered with deferoxamine over a period of six and fifteen weeks, respectively, receiving total doses of 270 and 675 mg of DFO. The concentrations of aluminum in serum and in tissues were compared with those found in other groups of animals undergoing aluminum suspension. The determination of iron in liver was also performed. Results indicate that in this experimental model the action of deferoxamine was preferential toward tone while it seemed lacking in the other examined tissues.
The effects of combined administration of ochratoxin A (OA) and aflatoxin B1 (AFB1) on the occurrence and the levels of residues of mycotoxins in poultry have been investigated. Male broilers and laying hens were fed from 14 days old with standard diets contaminated with 50 micrograms/kg OA and 50 micrograms/kg AFB1. Two groups of broilers and hens were withdrawn from contaminated feed at 37 and 88 days, respectively. At the time of sacrifice no significant lesions were found. Residues were compared with those found after administration of either toxin alone in former trials. Combined treatment resulted in higher content of OA in broiler livers (40 versus 5.0 micrograms/kg) and, to a lesser extent, in kidneys and skin, and of AFB1 in broiler liver and kidney (0.15 versus 0.02 microgram/kg and 0.40 versus 0.05 microgram/kg respectively). Laying hens showed smaller differences (0.20 versus 0.10 microgram/kg in liver and 0.32 versus 0.08 in kidneys). Withdrawal from treatment led to the almost complete disappearance of OA residues in broilers and in hens. These results show a synergistic effect of OA and AFB1, particularly in broilers.
The occurrence and amount of residues of ochratoxin A (OA) in poultry tissues and organs were investigated in a trial aimed at measuring the effects of contamination approaching the patterns more frequently found in natural situations (i.e., small doses of OA in the diet for long periods). Hubbard male broilers and laying hens were treated with an OA-contaminated feed (50 ppb) from the 14th day of age onward. Both groups were further divided into subgroups, some of which underwent continual treatment (64 and 169 days, respectively) and others that were withdrawn from administration (maximum 28 and 82 days, respectively). Determination of residues was performed by high performance liquid chromatography. Residues in liver were higher in broilers (up to 11.0 ppb) than in hens (1.5 ppb), whereas the reverse occurred in kidney (up to .8 and 5.8 ppb, respectively). Residues (.8 ppb) were also in hen thigh muscle but not in breast muscle. Residues of OA in poultry appear to be of possible public health concern. Suggestions for monitoring are given.
The enzymatic deamination of pure enantiomers of 2-methyl-1-4-diaminobutane catalyzed by diamine oxidases from two plants (Euphorbia characias latex and Lens esculenta seedlings) was studied to investigate the conformations of the active sites. The results suggest that, in 2-methyl-1-4-diaminobutane, the steric hindrance of methyl group is primarily involved in decreasing activity compared with 1-4-diaminobutane (Pu), the natural substrate of diamine oxidases. This approach suggests that by replacement of hydrogen with a methyl group in the physiological substrate, useful informations on the active site of diamine oxidases from different sources can be obtained.
In order to clarify the role of aluminum in the production of dialysis osteomalacia, an experimental study on rats has been carried out. Four groups of fifteen rats each have been treated daily with intraperitoneal injections of aluminum chloride for periods of up to three and half months.
High Aluminum concentration found in bones of hemodialyzed uremic patients has been described as the major responsible for the development of renal osteodystrophy (ROD) with severe osteomalacia. Histochemical (Ma82) and physical methods (Co81) have shown Al presence mainly at the mineralization front suggesting that the element has a specific action in inhibiting the calcification process. However, the occurrence of high Al concentration in bone of hemodialyzed patients whose ROD has prevalent hyperparathyroid changes rises several doubts about its role in the induction of osteomalacia. To study the actual influence of Al on bone mineralization, it has been administered to normal rats.