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PubMed2005

Optimization of selenium status by a single intraperitoneal injection of Se in Se-deficient rat: possible application to burned patient treatment.

In order to investigate the efficiency of a single selenium (Se) administration in restoring selenium status, Se and antioxidant enzymes were studied in an animal model of Se depletion. In Se-depleted animals receiving or not a single parenteral administration of Se, plasma, red blood cell (RBC), and tissue Se levels were measured concurrently with glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities. The oxidative stress was assessed by thiobarbituric acid-reactive species (TBARs), total thiol groups, glutathione, and tocopherol measurements. Our study showed that Se depletion with alterations in the antioxidant defense system (Se and GPx activity decreases) led to an increase of lipid peroxidation, a decrease of the plasma vitamin E level, and SOD activation. Sodium selenite injection resulted after 24 h in an optimal plasma Se level and a reactivation of GPx activity. In liver, brain, and kidney, Se levels in injected animals were higher than those in reference animals. However, this single administration of Se failed to decrease free radical damage induced by Se depletion. Therefore, in burned patients who exhibit an altered Se status despite a daily usually restricted Se supplementation, the early administration of a consistent Se amount to improve the GPx activity should be of great interest in preventing the impairment of the antioxidant status.

Animals↗
PubMed2000

Effect of chronic intraperitoneal injections of leptin on hypothalamic neurotensin content and food intake.

This study was intended for the investigation of the effects of chronic injections of leptin for 7 days on food intake and hypothalamic neurotensin (NT). Leptin treatment significantly reduced food intake [144.3+/-2.5 g (L) vs. 156.7+/-2.5 g (C); P=0. 002] and body weight gain [23.7 g+/-1.0 g (L) vs. 31.5+/-1.3 g (C); P=0.003]. NT concentration was lower in the lateral hypothalamus (LH) of leptin-treated rats than in the control ad libitum fed rats (-30%; P<0.05). The same diminution was observed in pair-fed rats (-27%; P<0.05). This diminution was therefore related to the decrease in food intake rather than to a direct effect of leptin. As the LH was the only area where NT was modified, it appears that among the hypothalamic nuclei involved in the regulation of feeding behavior it is the most sensitive area to a low energy depletion. Therefore, it might play a specific role in triggering the mechanisms necessary to restore body weight and/or energy balance.

Animals↗
PubMed1997

Apoptosis in the striatum of rats following intraperitoneal injection of 3-nitropropionic acid.

The present study investigated the mechanism of cellular degeneration within the striatum following administration of the mitochondrial toxin, 3-nitropropionic (3-NP) acid. Internucleosomal fragmentation typical of apoptosis was present in the DNA of cells from the striatum of 3-NP-treated rats. DNA fragmentation was also evident in this region by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling. The data suggest that striatal cells die by apoptosis following administration of 3-NP.

Animals↗
PubMed1975

The influence of l-methionine-d,l-sulfoximine on the labelling of acid soluble fraction and proteins of the brain cortex after intraperitoneal injection of 14c-leucine.

Methionine sulfoximine (MSO) inhibits the labelling of the acid soluble fraction and proteins of the brain cortex after the injection of 14C-leucine. The inhibition takes place even during the early stages after the injection of MSO, when no symptoms of paroxysms are observable. The action of MSO on the labelling of the acid soluble fraction and proteins in the brain cortex is obviously different from that in the kidney and liver. Whereas in the brain tissue MSO markedly influences the labelling of the free amino acid pool, in the kidney and liver it seems primarily affect the protein synthetic mechanisms. Also no decrease in labelling of the plasma acid soluble fraction was found on mice, treated with MSO. Experimental data support the idea, that the changes in the metabolism of proteins in the brain are not connected with the onset of the paroxysmal period.

Animals↗
PubMed1997

14C-labeled microcystin-LR administered to Atlantic salmon via intraperitoneal injection provides in vivo evidence for covalent binding of microcystin-LR in salmon livers.

The tissue distribution and clearance of radiolabeled microcystin-LR administered to Atlantic salmon via i.p. injection has been re-examined using uniformly 14C-labeled toxin. Significant differences were found to exist between these results and those obtained when fish received an i.p. injection of tritium-labeled dihydromicrocystin-LR. In addition, MeOH liver extracts were assayed by both phosphatase assay and 14C counts and the results compared with the total levels of incorporation determined by digestion and subsequent 14C counting of the same live tissues. An attempt to investigate the metabolism and to document the putative products was also undertaken. It was found that microcystin-LR was extensively metabolized to compounds that are more polar than the parent compound.

Animals↗
PubMed1999

Kidney leucocytes of rainbow trout, Oncorhynchus mykiss, are activated by intraperitoneal injection of beta-endorphin.

The immunomodulatory effects of beta-endorphin were studied by measurements of the production of superoxide anion, phagocytosis and chemotaxis of kidney phagocytic cells in rainbow trout, Oncorhynchus mykiss. The production of superoxide anion in phagocytic cells increased significantly in rainbow trout injected with chum salmon beta-endorphin. The responses were dose-dependent. The phagocytosis and chemotaxis also significantly increased in kidney phagocytic cells of rainbow trout injected with alpha-endorphin. These results show that beta-endorphin in rainbow trout activates the function of phagocytic cells in vivo.

Animals↗
PubMedDate not supplied

Effects of ethanol on energy balance of rats and the inappropriateness of intraperitoneal injection.

Energy balance of female rats that were either injected daily with ethanol or received the alcohol by gavage was determined and the results compared with saline animals. Food intake, feces elimination, and body weight were recorded daily. After a 20-day period of treatment the animals were sacrificed and the energy content of the carcasses and feces was determined by bomb calorimetry. The results indicated that ethanol-injected animals underwent an impairment in the energy balance, with losses in body weight and body energy. Also, there was a decrease in metabolized energy intake. The results of a group of saline rats pair-fed to alcohol-injected rats showed that the impairment of the energy balance was not only a consequence of the decreased energy intake, because the ethanol-fed animals had an energy balance that was worse than the one of the pair-fed rats, even though both had eaten the same amount of food. Nevertheless, when alcohol was given by gavage, no alteration in the energy balance parameters was detected. Macroscopic observation of the abdominal cavity showed adherences in the gut of the alcohol-injected animals. It is concluded that the ethanol by itself does not alter the energy balance; however, depending on the route of administration it could indirectly impair the energy balance.

Animals↗
PubMed1996

Differential diagnosis of malignant tumours in the abdominal cavity of rats after intraperitoneal injection of crocidolite or benzo[a]pyrene.

In our investigation (i.p. test), crocidolite and benzo[a]pyrene, both caused a progression from initially reactive, then autonomously transformed proliferation of myofibroblasts and undifferentiated mesenchymal cells to malignant, multidirectionally differentiated (desmin and ED-1 positive) fibro-histiocytic tumours. Immunohistochemically these tumours showed no morphological characteristics (for example co-expression of vimentin and keratin in spindle-shaped tumour cells) of human asbestos-associated malignant mesotheliomas. On the other hand many tumour cells induced by crocidolite and benzo[a]pyrene had an ultrastructural appearance resembling fibroblasts and myofibroblasts. These have been demonstrated in only a few desmoplastic and sarcomatous mesotheliomas in human beings. None of the tumours revealed the typical ultrastructural features of epitheloid or transitional mesotheliomas. Apparently, both carcinogenic substances induce the transformation of undifferentiated pluripotent mesenchymal cells in rat peritoneum, regardless of their localization in the submesothelial compartment or perivascular connective tissue (preferentially after crocidolite application) or in the connective tissue pseudocapsule of major benzo[a]pyrene containing beeswax/tricaprylin depots in the mesometrium and mesenterial fatty tissue. In this way asbestos fibres in this animal experiment do not seem to induce an arrest in differentiation of intermediate or immature mesothelial cells as supposed formerly, but rather affect undifferentiated mesenchyme cells and myofibroblasts. This is an explanation for the immunohistochemical expression of markers of muscular differentiation in these tumour cells, which is known to occur in human malignant fibro-histiocytic tumours. If supplementary immunohistochemical investigations with different keratin antibodies also fail to confirm the mesothelial differentiation of the tumours induced in our i.p. test, the decision to call them "mesotheliomas" should be reconsidered. Further immuno-transmission-electron microscopical investigations with intermediate filament or macrophage antibodies are needed to clarify whether the term malignant "fibrohistiocytic sarcoma", "mesenchymoma" or "mesothelioblastoma" would be more correct from the morphological point of view.

Abdominal Neoplasms↗
PubMed1997

P53 mutations in tumours induced by intraperitoneal injection of crocidolite asbestos and benzo[a]pyrene in rats.

Mutation analysis of the tumour suppressor gene p53 in tumours induced in the peritoneal cavity of rats revealed differences in the mutational pattern with regard to the carcinogenic substances applied. In tumours induced by benzo[a]pyrene a considerable amount of p53 mutations resulting in an altered protein structure could be detected. For the development of these tumours an escape from the p53 mediated cell cycle control can be assumed. However, in tumours of the same tumour type induced by crocidolite asbestos no mutations could be observed. Since there were even no spontaneous p53 mutations detectable in this tumour group, it is obvious that in these tumours the escape from cell cycle control does not take place via inactivation of p53. Therefore, it is concluded that the molecular mechanisms of carcinogenesis and tumour development in this tumour type depend on the type of carcinogen applied.

Animals↗
PubMed2005

Increased phosphorylation of Ser473-Akt, Ser9-GSK-3beta and Ser133-CREB in the rat frontal cortex after MK-801 intraperitoneal injection.

GSK-3beta is regarded as playing an important part in the pathogenesis of schizophrenia and the action of psychotomimetic agents. We observed phosphorylation of molecules associated with the GSK-3beta signalling pathway in the rat brain after MK-801 injection, which induces a schizophrenia-like state in humans. Ser9-GSK-3beta phosphorylation was increased after injection of 1 mg/kg MK-801 in the rat frontal cortex but not in the hippocampus or cerebellum. This increase peaked at 30 min and was maintained until 90 min after injection. The phosphorylation showed a dose-dependent increase up to 1 mg/kg MK-801, followed by a decrease at higher dosage. Furthermore, phosphorylation of Ser473-Akt and Ser133-CREB showed similar temporal, dose-dependent and regionally specific patterns with those of Ser9-GSK-3beta. However, phosphorylation of Dvl and Ser33-beta-catenin was not affected by MK-801. These results suggest that GSK-3beta phosphorylation by MK-801 may be associated with the Akt-GSK-3beta pathway rather than with the Wnt-Dvl-GSK3beta pathway.

Actins↗
PubMedDate not supplied

Oxidative DNA base damage in renal, hepatic, and pulmonary chromatin of rats after intraperitoneal injection of cobalt(II) acetate.

DNA base damage was studied in renal, hepatic, and pulmonary chromatin of male and female F344/NCr rats that had been given either 50 or 100 mumol of Co(II) acetate/kg body wt in a single ip dose and killed 2 or 10 days later. Control rats received 200 mumol of sodium acetate/kg body wt. Chromatin was isolated from organs and analyzed by gas chromatography/mass spectrometry with selected ion monitoring. The following 11 products derived from purine and pyrimidine bases in DNA were quantified: 5-hydroxy-5-methylhydantoin, 5-hydroxyhydantoin,5-(hydroxymethyl)uracil(5-OHMe-Ura),5- hyd roxycytosine(5-OH- Cyt),thymine glycol, 5,6-dihydroxycytosine,4,6-diamino-5-formamido-pyrimidine (FapyAde),2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua),7,8-dihydro-8-oxoadenine,2-oxoadenine, and 7,8-dihydro-8-oxoguanine. The response was organ-specific. Eight of the DNA base products in renal chromatin of Co(II)-treated rats (mostly 5-OH-Cyt and other pyrimidine products), five in hepatic chromatin (mostly FapyGua and other purine products), and two in pulmonary chromatin (5-OHMe-Ura > FapyAde) were increased by 30% to more than 200% over control levels with increasing Co(II) dose. The renal and hepatic, but not pulmonary, DNA base damage tended to increase with time. No significant differences in response were found between male and female rats. The bases determined were typical products of hydroxyl radical attack on DNA, suggesting a role for this radical in the mechanism(s) of DNA damage caused by Co(II) in vivo. Some of these bases have been shown previously to be promutagenic. The present results imply involvement of oxidative DNA base damage in Co(II)-induced genotoxic and carcinogenic effects.

Acetates↗
PubMed1992

Sustained delivery of interleukin-2 from a poloxamer 407 gel matrix following intraperitoneal injection in mice.

Parenteral delivery of recombinant biologic response modifiers (BRMs) remains a challenge because of the brief intravascular half-life of most recombinant proteins and their associated rapid clearance from the circulation. Recombinant derived interleukin-2 (rIL-2) was formulated with Pluronic F-127, N.F. (poloxamer 407, N.F.) and the biological activity determined vs time at 4, 22, and 37 degrees C. As assessed by rIL-2-induced peripheral blood lymphocyte (PBL) uptake of [3H]thymidine, storage of rIL-2/poloxamer 407 (33% w/w) for 72 hr at 4 and 22 degrees C did not result in an overall negative slope of the [3H]thymidine vs time profiles. However, storage of an rIL-2/poloxamer formulation at 37 degrees C for 72 hr resulted in an approximate 15% reduction in the biological activity as assessed by [3H]thymidine incorporation. As assessed by bioassay ([3H]thymidine uptake), the cumulative percentage rIL-2 released in vitro at 22 degrees C after 8 hr from rIL-2/poloxamer 407 matrices containing either 30% (w/w) or 35% (w/w) poloxamer 407 was 81.8 +/- 1.7 and 82.1 +/- 4.7%, respectively. When ELISA was used to determine the amount of rIL-2 released vs time, the corresponding values for the cumulative percentage rIL-2 released were 82.6 +/- 10.1 and 40.9 +/- 8.8%. Cytotoxicity of rIL-2 stimulated PBLs cultured with poloxamer 407 (0.17%, w/w) toward malignant Daudi cells was significantly (P less than 0.05) enhanced compared to controls. Finally, mice injected with the rIL-2/poloxamer 407 formulation (1 x 10(5) U/inj. q.d. x 3 days) demonstrated a bioequivalent effect of rIL-2-induced natural killer (NK) cell activity in vitro toward malignant murine YAC-1 cells at one-half the standard exogenously administered dose of rIL-2 known to generate enhanced NK lytic activity in mice (1 x 10(5) U/inj. b.i.d. x 3 days). No untoward systemic side effects were observed for mice injected i.p. with polymer vehicle alone (30%, w/w) (0.15 ml q.d. x 3 days), pH 7 phosphate-buffered saline (PBS) (0.15 ml q.d. x 3 days), rIL-2 formulated with poloxamer 407 (30%, w/w) (1 x 10(5) U/0.15 ml q.d. x 3 days and 0.5 x 10(5) U/0.15 ml q.d. x 3 days), or rIL-2 dissolved in PBS (1 x 10(5) U/0.15 ml b.i.d. x 3 days).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗