[Free pyrimidine and purine content in rat liver and incorporation of NaHC 14 O 3 under the action of a single intraperitoneal injection of orotic acid].
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Parameters of liver metabolism were studied in the isolated perfused rat liver 5 days after a standard skin burn or an i.p. injection of a specific cutaneous burn toxin. Decreased values of the energy quotient ATP/ADP compared with normal controls were found. The absolute content of adenonucleotides was unchanged. The excretion of glucose and urea was also decreased in both groups and glucose synthesis after a lactate load was only slightly stimulated. The results show a direct influence of a burn toxin on hepatic metabolism suggesting a possible disturbance of oxydative phosphorylation.
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The response of peritoneal cells to transplantable Novikoff hepatoma was studied in immunized and nonimmunized inbred male SD rats to elucidate the role of macrophages in syngeneic tumor rejection. Specific immunization was induced by double sc challenge with viable tumor cells. Peritoneal cells were harvested by lavage at intervals of 6 hours and 1, 2, 3, 4, and 9 days after ip tumor injection. Some of the lavage fluid was used to determine the total number of cells, and the remainder was prepared for ultrastructural study. Different counts were made at the electron microscope level, and the ultrastructures of macrophages and tumor cells were studied. The results indicated that during the early intervals after tumor injection, the numbers of macrophages and lymphocytes were significantly increased in immunized animals. The mononuclear cells accumulated more slowly in the peritoneal cavities of nonimmunized rats. Morphologic heterogeneity was observed in the macrophage population of immunized rats up to day 4. Concurrent with these changes in macrophages were the decreased mitotic activity and ultrastructural alterations in tumor cells followed by their complete disappearance. In nonimmunized animals tumor cells proliferated actively and by day 9 constituted 85% of the peritoneal population.
I.p. injection of glass fibres to rats of different strains resulted partly in different tumour rates. Young rats showed more marked coalescence and earlier growth of tumours but also earlier mortality without tumours, as compared with older rats. Haemorrhagic ascites from tumour-bearing rats induced tumours after i.p. injection. Tumours were also obtained after i.p. injection of fibres in European hamsters and rabbits, but these species are less susceptible than rats. Histological studies in rats show that fibrosis is not an absolute requirement for the development of a fibre-induced mesothelioma. After intratracheal instillation of either crocidolite or glass fibres in European hamsters, the respective fibres showed up in the diaphragm and in the spleen.
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A study was made of the adrenaline and noradrenaline content in the blood, myocardium and adrenals of 74 male Wistar rats. Four series of experiments were conducted with administration of noradrenaline alone and noradrenaline after premedication with arfonad (ganglion-blocking agent) or rausedil (reserpine drug). Distilled water was used in control experiments. The content of adrenaline and noradrenaline in blood and tissues was shown to change 45 seconds after noradrenaline administration and to return to normal by the 7th minute. Correlation of the catecholamine content in rat blood and tissues with morphological changes in the myocardium recorded in the analogous series of experiments has shown that the increased content of catecholamines in bloods is one of the most important factors in the pathogenesis of myocardial injury since the diminution of their content during ganglionic blockade is associated with a reduced heart injury. The noradrenaline content in the myocardium does not correlate with the severity of myocardial injury.
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OBJECTIVE: The protection rate of inoculation with BCG vaccine is only 50 percent, and most of patients with tuberculosis had a history of BCG vaccine inoculation. Adenosine (ADO) has an immunomodulating effect; it promotes immune reaction by increasing number of macrophage and enhancing phagocytosis. The present study was designed to investigate if combined use of adenosine with BCG enhances the anti-Mycobacterium tuberculosis effect of macrophage in mice. METHODS: Fifty BALB/C mice were divided randomly into 3 groups: BCG group (n = 21), BCG plus ADO group (n = 21) and control group (n = 8). The mice in BCG and BCG plus ADO groups were inoculated with 0.1 ml BCG intradermally and the mice in BCG plus ADO group were injected intraperitoneally with ADO 30 mg/(kg.d) for 5 days. The mice in BCG group and control group were injected with NS 0.1 ml/d for 5 days. Six weeks after the last injection, all mice were challenged with intravenous 1 x 10(6) CFU human Mycobacterium tuberculosis virulent strain. After challenging, lung and spleen specimens were taken at the 10th, 20th and 30th days from the mice of BCG and BCG plus ADO groups and at the 30th day from mice in control group. The pathological examinations of lung and spleen sections were performed after HE staining and acid-fast staining, and detection of cell apoptosis was also performed. RESULTS: Consolidation with neutrophil infiltration was found in most of the lung tissue taken at the day 30; there were a lot of tuberculous granulomas and Mycobacterium tuberculosis in the lungs of control group. The alveolar septum in BCG gradually became wide and in interstitium lymphocyte infiltration dominated, and there were less tuberculous granulomas but there were large number of Mycobacterium tuberculosis in the lungs from 10th to 30th days after challenging. The widening of alveolar septum and consolidation of lung tissue in BCG plus ADO group became milder with monocytes infiltration, and there were few tuberculosis granulomas and Mycobacterium tuberculosis in the lungs from 10th to 30th days after challenging. CONCLUSION: ADO could increase the number of monocyte-macrophages and promoted anti-bacterial effects of these cells.
Cadmium is known to be a carcinogenic metal that especially its compounds have sufficient evidence in both humans and experimental animals beneath its environmental effects. Testis tissue is highly sensitive to the effects of cadmium. It is proposed that cadmium also increases oxygen derived free radicals and lipid peroxidation. As indicators of oxidative DNA damage, 6 oxidative DNA bases were determined by using Gas Chromatography/Mass Spectrometry-Selected Ion Monitoring technique. 45 Sprague-Dawley rats (225-300 g) were used as experimental animals and were divided into 3 groups of 15 rats. A single 2 mg NaCl/kg body wt, 0,5 and 1,25 mg CdCl2/kg body wt were injected intraperitoneally to control, low and high dose groups, respectively. 5-OH Cytosine, 8-OH Adenine and Fapy Guanine lesions were elevated significantly in high dose group in the first day. A clear dose-response relationship was seen between dose groups and 8-OH Adenine levels related with time in all periods. There was a significant dose-response relationship in 2-OH Adenine, Fapy Guanine and 8-OH Guanine, especially in the second week suggesting the inhibition of XPA protein by cadmium after first week. In contrast, the observation of a significant decrease of 5-OH Cytosine levels after first week showed that cadmium could not affect the enzymes repairing the cytosine base lesions.
The effect of parenterally administered ethanol on the percutaneous absorption of phencyclidine hydrochloride was investigated using the intact hairless (SKH, hr-1/hr-1) mouse as a model. Four hours after topical application of phencyclidine hydrochloride, the mean phencyclidine concentration (129.2 ng/g) in excised liver was significantly lower in mice that had received ethanol by intraperitoneal injection than in mice injected intraperitoneally with water (1730.1 ng/g) (p less than 0.01). When phencyclidine hydrochloride was administered by intraperitoneal injection there was no statistically significant difference between the mean concentration in liver (3442.5 ng/g) for ethanol-treated mice and that (3030.3 ng/g) for the control mice (p greater than 0.10), indicating that the observed difference was not due to enhancement of phencyclidine metabolism by ethanol. These findings suggest that ethanol inhibits the percutaneous absorption of phencyclidine hydrochloride.