AIMS: Uveal malignant melanoma is the most common intraocular tumor. The aim of this study was the analysis of bcl-2 oncoprotein expression in this tumor type. The melanomas were evaluated according to tumor location and patient age and sex. The relationship between bcl-2 expression and histological type, clinicopathologic stage and the presence of a set of predetermined morphological parameters was analyzed. METHODS: The study involved 39 patients with ocular melanomas treated with surgery alone between 1983 and 1997. Formalin-fixed, paraffin-embedded tissues were treated with anti-bcl-2 antibody (Dako No M0887). Immunolocalization of the bcl-2 oncoprotein was performed using the labeled streptavidin biotin (LSAB) method. bcl-2 expression in neoplastic cells was evaluated in a semiquantitative manner: lack of reactivity was defined as bcl-2 negative, reactivity present in less than 30% of cells as low bcl-2, and reactivity in more than 30% of cells as high bcl-2. The percentage of cells with a positive reaction was assessed independently by two pathologists, and the results were subjected to statistical analysis using Fischer's exact test. RESULTS AND CONCLUSION: No statistically significant correlation was found between the expression of bcl-2 oncoprotein and the clinicopathologic features analyzed. However, the high percentage of tumors with positive expression of this oncoprotein suggests that it plays a significant role in the biology of uveal melanoma.

Female↗

PubMedDate not supplied

Experimental model of hepatic venoocclusive disease (VOD) caused by dactinomycin--preliminary report about hepatoprotective effect of amifostine.

UNLABELLED: The purpose of the study was elaboration of the experimental model of hepatic venoocclusive disease (VOD) induced by dactinomycin and investigation of possible hepatoprotective effects of amifostine and heparin individually or in combination with dexamethasone. 198 Wistar strain male rats were used in the trial in two series of experiments. In the first series the experimental model of VOD induced by dactinomycin was elaborated on the group of 18 animals (divided into 3 groups receiving intraperitoneally isotonic salt solution, dactinomycin or nitrosamine). Nitrosamine--a well-known agent causing VOD--was used as positive control. Open biopsies of the liver and blood collections were repeated in order to determine liver enzymes' concentrations. Histopathological examinations demonstrated that dactinomycin caused liver lesion corresponding with VOD picture. Second series of animals was divided into 6 groups receiving the following drugs: I--0.9% NaCl solution, II--dactinomycin (ACT), III--ACT + fraxiparine s.c., IV--ACT + fraxiparine + dexamethasone, V--ACT + amifostine. Five animals from each group were sacrificed on the 3rd and 7th day after each cycle of drug administration. Blood was drawn in order to determine the following: AspAT, AlAT, Falk, GGTP and LDH. Intravital wedge biopsies under anesthesia with the use of inactin were also performed. Liver samples were stained with the use of H&E, p. a. S and Gomory's techniques. We did not find significant differences in liver enzymes' levels between the groups. Pathological changes corresponding with VOD picture of different intensification were found in liver samples from all the rats receiving ACT. Changes became more and more intensive after consecutive cycles. Lesion of central veins' and liver sinusoids' endothelium dominated. Fraxiparine administered individually or in combination with dexamethasone did not prevent the lesion. Administration of amifostine before ACT decreased pathomorphological changes in liver. Dactinomycin caused homogenous subclinical liver lesion corresponding with VOD. It may also occur in children receiving ACT in the course of nephroblastoma's treatment. But probably the changes are too subtle to manifest themselves clinically with exception of patients particularly sensitive (for example after previous radiotherapy). Lack of differences observed in liver enzymes' levels between the groups supports the explanation. Markers of lesion of liver vessels' endothelium should be looked for to make more specific diagnostics of VOD possible. Hepatoprotective properties of amifostine need further studies. CONCLUSIONS: 1. It is possible to create the experimental model of VOD induced by dactinomycin administration. 2. Amifostine seems to act hepatoprotectively to liver lesions caused by dactinomycin.

Alanine Transaminase↗

PubMedDate not supplied

[Effect of immunomodulating drugs on the release and activities of lysosomal proteinases of the liver of rats with ethanol poisoning].

Increased activity of cathepsin A and D in the cytosol fraction and homogenate of the liver of rats intoxicated for 4 weeks with ethanol (0.6 g/100 g of the body weight) was found. The cytosol cathepsin A and D activities were unaffected under the influence of Levamisole and isoprinosine++. Encorton reduced the activity of both cathepsins in the cytosol fraction while it did not diminish their activities in the liver homogenates. Encorton, and to a markedly lesser degree, Levamisole and isoprinosine++ caused a regression of vacuolar degeneration and of necrotic lesions and an increase in the number of glycogen granules in the livers of ethanol-intoxicated rats.

Adjuvants, Immunologic↗

PubMedDate not supplied

[Effect of cysteine on protein metabolism in the liver of rats with ethanol-induced liver damage].

Rats intoxicated with ethanol at the dose of 0.6 g/100 g of the body weight during 4 weeks were fed on standard diet and the one containing 0.125, 0.25 and 0.5% L-cysteine. Intoxication of rats fed standard food causes an increase in the activity of cathepsin D and gamma-glutamyl-transpeptidase in the liver and an increase in the activity of alanine aminotransferase and gamma-glutamyl-transpeptidase in the blood serum. Consuming by rats food containing small and medium quantity of cysteine causes normalization of the activity of all enzymes, whereas consuming food containing large quantity of cysteine does not give such effect.

Alanine Transaminase↗

PubMedDate not supplied

[Histopathological evaluation of protective effect of L-cysteine in ethanol-induced liver damage in rats].

Rats fed standard diet were intoxicated during 4 weeks with ethanol at the dose of 0.6 g/100 g of the body weight. This poisoning causes vacuolar degeneration, disappearance of glycogen granules, steatosis of hepatocytes and focal necrosis changes in the liver. The intake of food with cysteine at the dose of 0.012 and 0.024 g/100 g/24 hrs markedly prevents histopathological changes in the liver of rats intoxicated with ethanol. Larger amounts of cysteine (0.044 g/100 g/24 hrs) intensify histopathological changes caused by ethanol in the liver of rats.

Alcohol Deterrents↗

PubMedDate not supplied