Abstract. The aim of the study was to verify whether an increased supply of vitamins E and C prevents the detrimental effects of ozone on the testes. The experiment was performed on 5-monthold rats exposed to ozone (0.5 ppm) for 50 days (5 h daily). Simultaneously, the animals were injected with the vitamins in 5-day intervals and at different doses (0.5, 1.5, 4.5, 5 and 15 mg of vitamin E; 0.5, 3, 9, and 50 mg of vitamin C; or both vitamins together, respectively). Gonad sections were PAS stained. In the ozonized males, depletion of germ cells occurred. In the vitamin E groups, the testes were comparable to the controls, excluding the 0.5-mg-dose vitamin E group in which perivascular fibrosis and intertubular hyalinization were observed. In the vitamin C groups, intertubular hyalinization, partial arrested spermatogenesis, and desquamation of the seminiferous epithelium appeared proportionall to the vitamin dose. Additionally, premature spermiation was found at a vitamin C dose of 50-mg. In the rats injected with both vitamins, hyalinization and fibrosis appeared in addition to partial arrest of spermatogenesis and vacuolar degeneration. In conclusion, vitamin E protects against the detrimental effects of ozone in rat testes irrespective of the dose applied. This was not observed for vitamin C. Moreover, administration of higher doses of vitamin C intensified the damage to the testes caused by ozone.

This study evaluated the morphology and immunohistochemistry of 85 canine cutaneous histiocytic tumours. The tumours were classified morphologically as either canine cutaneous histiocytomas (71 tumours) or canine cutaneous histiocytic sarcomas (14 tumours). The immunohistochemical analysis was conducted on paraffin sections using an antibody panel (against MHCII, CD18, CD79αcy, CD3 and E-cadherin). Histochemical staining with toluidine blue and Gomori silver impregnation was also performed. A follow-up was conducted via surveys. The histiocytic origin of the tumour cells was confirmed in 65 of the canine cutaneous histiocytomas and in 4 of the canine cutaneous histiocytic sarcomas. The tumours that had been misdiagnosed as canine cutaneous histiocytomas included plasmacytomas, epitheliotropic T-cell lymphomas and undetermined entities. The tumours misdiagnosed as canine cutaneous histiocytic sarcomas included plasmacytomas and non-epitheliotropic T-cell lymphomas, but the majority of them remained undetermined. The canine cutaneous histiocytomas showed MHCII, CD18 and E-cadherin expression, but in several of the tumours, the expression of CD18 or E-cadherin was confirmed in only a small percentage of the tumour cells. The regressing canine cutaneous histiocytomas showed increased T- and B-lymphocyte infiltration, a decreased mitotic index, transport of the MHCII molecules from the cytoplasm to the cell membrane and loss of E-cadherin expression in the tumour cells. The canine cutaneous histiocytic sarcomas showed both high morphological diversity and expression of MHCII and CD18. Two of the evaluated histiocytic sarcomas also showed expression of E-cadherin. In conclusion, immunohistochemistry, including analysis of MHCII, CD18 and the lymphocytic markers CD3 and CD79, should be performed for the diagnosis of canine cutaneous histiocytic tumours. The expression of E-cadherin in canine cutaneous histiocytic sarcomas suggests an origin of the tumour cells among Langerhans cells.

No abstract

Ultrastructural changes of liver and kidneys of cockerels exposed to mercuric chloride and subsequent interaction with methylobromofenvinphos (IPO 63 compound) were studied. Group A birds were treated for 4 weeks with 300 ppm mercuric chloride in drinking water; Group B birds were treated for 4 weeks with mercuric chloride followed by single oral dose of 240 mg/kg of IPO 63; Group C 240 mg/kg IPO 63 only; and Group D, unexposed controls. Hepatocytes of mercury-IPO 63 interaction group B showed large lysosomes containing myelin bodies, swollen mitochondria with cristeolysis, dilated endoplasmic reticulum and numerous vacuoles containing granular material. Mercury-intoxicated birds showed similar but less severe changes, whereas IPO 63-treated birds showed accumulation of glycogen granules, fat droplets, and few lysosomal bodies as well as other changes. Renal corpuscles of kidney from mercury-IPO 63 interaction birds revealed minor ultrastructural changes as vacuolation, swollen mitochondria of podocytes and slight thickening of the glomerular basement membrane. Proximal tubular cells showed extreme damage such as, microvillar loss, dilation of endoplasmic reticulum, accumulation of lysosomal bodies, glycogen granules, myelin figures, swollen mitochondria with granular material, numerous vacuoles containing degenerated membranous organelles and distorted, pyknotic nucleus with marked dilation of nuclear membrane. Mercury intoxicated birds showed similar but less pronounced changes in tubules. These observations suggest that the effect of mercuric chloride toxicity and then interaction with an organophosphorus insecticide causes extreme damage to hepatic and renal cells that appears to be additive.

The purpose of this study was to examine the safety of the long-term application of QuikClot Combat Gauze, ChitoGauze PRO and Celox Gauze using a swine model. The study was conducted on nine pigs weighing approximately 30 kg, which were randomly divided into three groups. Under deep anesthesia, the pigs underwent complete transverse cutting of the femoral artery in the groin region. Hemostatic dressings were left in the wound for 24 hours. The animals were euthanized 24 hours after dressing application. In each group, macroscopic and microscopic severe changes and shock symptoms were observed in the lungs, liver, kidneys and heart. Fibrino-gaseous embolic material was found in the pulmonary artery of each group and in the lung vessels of the animals from the ChitoGauze PRO and Celox Gauze groups. In conclusion, the long-term application of the evaluated hemostatic dressings has the risk of coagulopathy and reaching the progressive stage of shock. The residues from the hemostatic dressings can ingress into the systemic circulation, thereby increasing the risk of embolus formation. Because of these harmful effects, the evaluated hemostatic dressings are not appropriate for long-term use. Future studies are needed on the consequences of the long-term application of these hemostatic agents.