Despite the increasing use of amorphous silica nanoparticles (SNPs) in biomedical applications, their toxicity after intravenous administration remains a major concern. We investigated the effects of single 7 mg/kg intravenous infusions of 13 nm SNPs on hemodynamic parameters in rats. Hematological and biochemical parameters were assessed at 7, 30, and 60 d post treatment. Silicon content in the liver, lungs, heart, and kidney was analyzed, as well as tissue histology with special emphasis on mast cell (MC) content. SNP infusion had no effect on hemodynamics, nor did it alter hematological or biochemical parameters. SNP retention in the liver was conspicuous for up to 60 d. Among the other organs analyzed, silicon content was significantly increased only in the lung at 1-h post infusion. Despite the relatively low dose, SNP administration caused extensive liver remodeling, including the formation of multiple foreign body-type granulomas starting 7 d post treatment, and subsequent development of fibrosis. Histopathological changes in the liver were not preceded by hepatocyte necrosis. We found increased MC abundance in the liver, lungs, and heart starting on day 30 post treatment. MC recruitment in the liver preceded fibrosis, suggesting that MCs are involved in liver tissue remodeling elicited by intravenously administered SNPs.

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The nature and specificity of the damaging effect of an Anthio-tarred turpentine combination and the changes it produces are studied in acute, subacute, and chronic experiments on cats. Anthio, a compound capable accumulating in adipose tissues and destroying lipidcontaining structures (for example, surfactant), induces characteristic destructive effects on lung alveoli and causes dystelectasis and the formation of ectases, which are observed in acute experiments. The ectases contain an oxyphilic serous exudate and microfocal lymphoid-cellular clusters in the alveolar wall and are characterized by microcirculatory disorders such as edema, capillary and venous stases, and microhemorrhages. Study of the combined effect of Anthio and turpentine shows that the Anthio-induced destruction is persistent and probably creates conditions for secondary damaging factors which aggravate the pathological process and broaden the spectrum of the morphological alterations characteristic of acute pneumonia. Key Words: Anthio; turpentine; pneumonia; surfactant; ectasesLung pathology has been studied in acute animal experiments reproducing pneumonia induced with the organophosphorus compound (OPC) Anthio and turpentine, which cause severe pathology in human beings [1,2,5,6]. Chronic experiments show that Anthio has a moderate toxicity and is eliminated primarily via the lungs. Peribronchial atelectases, reduced or emphysemic alveoli, focal thickening of the interalvetolar septa due to lymphoid-cellular infiltrates and capillary plethora, and perivascular accumulations of lymphoid-histiocytic cells have been observed in the lungs. On days 15-20, major bronchopulmonary destruction and the formation of bronchiectases have been documented [2,3]. Anthio induces circulatory disorders and concomitant destructive changes in the myocardium, liver, kidneys, adrenals, and brain [6]. Under experimental conditions, tarred turpentine, used as an irritant [4,5,11], induces changes characteristic of spontaneously developing pneumonia and causes damage to the respiratory epithelium and some structures of the intraorganic (microcirculatory) component of the pulmonary vascular bed which form the air-blood barrier [11]. Destruction of this barrier results in serous exudation into the alveolar lumen [4], with concomitant pronounced hemodynamic disorders. This indicates the prevalence of the alterative component in the set of pathomorphological responses typical of pneumonia.The aim of this study was to examine the damaging effect of Anthio, tarred turpentine, and their combination in acute and subacute experiments. MATERIALS AND METHODSExperiments were performed on cats of both sexes weighing 2.8-4.3 kg. The animals were maintained on a full-value diet. Prior to the experiments, they were