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Usually practicing veterinarians and animal keepers have to deal with inadequate supplementation of copper which causes deficiency diseases. However, instead of curing, the consequential intake of copper is likely to cause copper intoxication. Copper poisoning is observed particularly frequently, in sheep - the most sensitive domestic animal to copper toxicity. In most cases, sheep undergo chronic exposure to copper causing liver necrosis and resulting in massive haemolysis, haemoglobinuria and eventually in renal failure. The observed symptoms have an acute character and a set of them is called haemolytic crisis. The pathogenesis, signs and diagnosis of this syndrome are described in this article.
There is observed increasing pollution of environment by nitrosocompounds. Acute intoxication of animals by nitrosocompounds lead to necrosis and chronic exposure to neoplasm. We have little information on the influence of nitrosocompounds on metabolism of glycoconjugates (glycoproteins, glycolipids and proteoglycans) in animals. The aim of our work is evaluation the influence of exposure of rats for 10 and 90 days to N-nitrosodimethylamine (NDMA), on activity of lysosomal exoglycosidases (enzymes hydrolysing terminal sugars in oligosaccharides) in the alimentary tract. It was found that intoxication of rats with NDMA increased specific activity of N-acetyl-b-hexosaminidase, b-galactosidase and a-mannosidase in majority of tissues of rat alimentary tract. Damage the cells of alimentary tract by NDMA or its metabolites, increase activity of exoglycosidases, because damaged tissue elements must be removed by catabolic enzymes before restoration processes can start.
The effect of exposure to cadmium (Cd) on the function and structure of the thyroid with parathyroids and a relationship between Cd accumulation in these glands and their damage were studied on a male rat model corresponding to human exposure. For this purpose, male rats were treated with Cd in drinking water at concentration of 5 and 50 mg Cd/dm³ for 12 and 24 weeks. The function of the thyroid was evaluated based on the measurement of serum concentrations of triiodothyronine (T₃) and tetraiodothyronine (T₄), and immunohistochemical identification of hormones such as calcitonin (CT), calcitonin-gene related peptide (CGRP) and somatostatin (ST). To assess the parathyroid function immunohistochemical reaction for parathyroid hormone-related peptide (PTHrP) was performed. Histological structure of the thyroid and parathyroid glands was evaluated in a light microscope. Rats exposed to 5 and 50 mg Cd/dm³ showed changes in the epithelium of follicular cells, intensified remodeling of the glandular structure of the thyroid, mononuclear cell infiltrations in connective tissue and pale staining of colloid. Hypertrophy and hyperplasia of endocrine parathyroid cells were evident.The intensity of reactions for CT, ST, CGRP and PTHrP was weakened. Exposure to Cd had no effect on the T₃ and T₄ serum concentrations, except for a marked increase in the concentrations of both hormones after 24 weeks of exposure to 50 mg Cd/dm³ . All the Cd-induced changes were much more advanced at exposure to 50 mg Cd/dm³ than 5 mg Cd/dm³ . The seriously disturbed structure and function of the thyroid and parathyroids at a low Cd concentration (0.087 ± 0.005 µg/g) in these glands suggests that the damaging Cd influence may be due to its indirect rather than direct action. Based on the results it can be hypothesized that a human body chronically exposed to moderate and relatively high Cd levels may be at risk of damage to the thyroid and parathyroid glands.
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Chromosomal aberrations in humans induced by benzene

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Adverse effects associated with occupational exposure to benzene have often been reported in humans. It has been shown, that benzene causes chromosomal aberrations, sister chromatid exchanges and micronuclei in lymphocytes of exposed workers. In addition to evidence by conventional cytogenetic methods, the genotoxic effect of benzene has also been proved by a more specific approach based on fluorescence in situ hybridization with DNA probes. In the present paper, the nature of benzene-induced chromosomal aberrations and supposed consequence on human health is reviewed. The new possibilities in chromosomal alterations identification by molecular cytogenetic methods are also presented.
We previously discovered that a 4-wk course of indomethacin delivered to rats with acetic acid ulcers resulted in production of "unhealed gastric ulcers" that persisted for up to 12 wks after treatment cessation. The present study examined the mechanism underlying such "unhealed gastric ulcers" with biochemical and histological procedures. "Unhealed gastric ulcers" were induced with a 4-wk indomethacin treatment (1 mg/kg, twice daily) in rats with acetic acid ulcers. Two and 4 wks after treatment cessation, ulcer size was significantly larger in rats receiving indomethacin compared with control animals. Ulcerated tissue prostaglandin E2 levels were significantly lower during indomethacin treatment, but the levels tended to increase after treatment cessation compared with levels measure in the group receiving vehicle. Myeloperoxidase activity levels were significantly higher during indomethacin treatment; such levels persisted after treatment cessation. Histologically, greater degrees of fibrosis and neutrophil accumulation, as well as a lesser degree of angiogenesis were observed in the "unhealed gastric ulcers" compared to ulcers that healed in a normal fashion. It was concluded that severe fibrosis, persistent neutrophil infiltration, and poor angiogenesis in the ulcer base might represent factors involved in the mechanism underlying production of "unhealed gastric ulcers".
We observed the effect of cadmium (Cd group) and cadmium+zinc (Cd/Zn group) in the liver of turkeys after a 71-day exposure. The experimental birds were divided to three groups; control group (Control), group exposed to cadmium (group Cd) as CdCl₂ (aqueous solution, 0.5 mg/kg feed); and group Cd/Zn exposed to the same dose of cadmium as Cd group plus zinc as ZnSO₄ (aqueous solution, 90 mg/kg feed). Light and electron microscopy revealed pronounced changes in the liver of turkeys from the Cd group, such as hyperaemia, dilatation of sinusoids and accumulation of inflammatory cells, including macrophages, heterophils, and lymphocytes in sinusoids. Necrotizing hepatocytes were observed sporadically. The ultrastructural changes included swollen mitochondria with injured cristae, dilated cisternae of rough endoplasmic reticulum, and damaged intercellular contacts between hepatocytes. In the Cd/Zn group, Zn was not able to completely protect the liver, but the changes were less pronounced. The specific activity of superoxide dismutase was significantly increased in the Cd group. Glutathione peroxidase was significantly increased in all experimental groups. In the Cd/Zn group, zinc co-administration had a protective effect on the activity of antioxidant enzymes. Exposure of turkeys to cadmium did not affect the content of TBARS in the liver.
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