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At least 397 records · Page 22Linked to original sources
PubMed2001

Apoptosis of antigen-specific T cells induced by oral administration of antigen: comparison of intestinal and non-intestinal immune organs.

Oral administration of a protein without adjuvant brings about oral tolerance (systemic hyporesponsiveness) to that protein by mechanisms such as antigen-induced apoptosis. We monitored the number and apoptosis induction of CD4+ T cells in antigen-specific T cell receptor transgenic mice fed the antigen ovalbumin to identify where events leading to oral tolerance occurred. The antigen was distributed throughout the body, causing apoptosis and a decrease in cell number of CD4+ T cells in most of the lymphoid system: the spleen, peripheral lymph nodes, and the thymus which was not previously reported to be affected. Although apoptosis was induced in the Peyer's patches, the cell number did not change. Unexpectedly, T cells in the mesenteric lymph nodes did not undergo apoptosis; instead, they were more numerous as compared to that in the case of control animals not administered the antigen. The results suggested that the orally administered antigen activated the intestinal immune system, while it induced immune tolerance in other sites.

Administration, Oral↗
PubMed1991

Autoradiographic examination of the organ distribution of 14C-labelled pentamidine in rats after intravenous and inhaled administration.

The organ distribution of 14C pentamidine was studied in Sprague Dawley rats by means of whole-body autoradiography following intravenous and inhaled application of pentamidine (Pentacarinat, CAS 140-64-7). The distribution time after intravenous administration of 5 mg pentamidine per kg rat was 30 min, 6 h, 24 h, and 7 days, respectively. The corresponding times after administration of aerosolized pentamidine were 30 min and 24 h. The distribution of radioactivity was also determined by measuring radioactivity in punch specimens of 100 microns sections. Besides renal excretion, the excretion of pentamidine in the bile and via the salivary glands was assessed by autoradiography. Further target organs included the spleen and the bone marrow. As early as after 30 min no radioactivity was detectable in the blood vessels. A lack of radioactivity in the brain tissue with accumulation of pentamidine in the meninges suggests that pentamidine does not cross the blood/brain barrier. Following intravenous administration the lung uptake of pentamidine was relatively low. However, increased drug concentrations were recorded in the bronchial system. The elimination time of pentamidine from the target organs was long. Lung pentamidine concentrations remained almost unchanged for a period of 7 days. After inhaled administration high levels of pentamidine were measured in the lung. 14C pentamidine was also located in the oropharyngeal and gastrointestinal tract, the drug stemming from pentamidine ingested or licked off the skin by the animals. No further target organs were verifiable. From the pharmacological point of view, these studies prove the advantages of pentamidine aerosol in the treatment of Pneumocystis carinii pneumonia (PCP) and provide information on extrarenal excretion mechanisms and deep compartments.

Administration, Inhalation↗
PubMed2004

Effect of nickel(II) chloride on iron content in rat organs after oral administration.

The effect of oral administration of nickel(II) chloride on iron content in serum and certain body organs of rats was investigated. The male adult rats were given 300 and 1200 ppm Ni in drinking water for 90 d. The iron content in serum, liver, kidney, lung, spleen, and brain was analyzed 30 and 90 d postexposure. The hemoglobin, hematocrit, and body and organ weights were also measured. Nickel given in drinking water led to a pronounced increase in iron content in serum and the liver, as compared to control rats. This effect was related to Ni concentration in the water. There was not great time-dependent difference in the iron content as a response to continuous nickel treatment, except the lung of 1200-ppm Ni-treated rats. In relation to hematological parameters, Ni supplementation did not affect any of them. Body weight significantly decreased, and lung weight was significantly increased in 1200-ppm Ni-treated rats. The results of this study indicate that nickel ingestion (300 and 1200 ppm in the drinking water) induces the iron uptake by serum and some organs of rats. The highest amount of iron was found in the liver of all exposed animals, and the time-dependent difference in iron content was observed in the lung of 1200-ppm Ni-treated rats.

Administration, Oral↗
PubMed1997

Evaluation of renal function in rhesus monkeys and comparison to beagle dogs following oral administration of the organic acid triclopyr (3,5,6-trichloro-2-pyridinyloxyacetic acid).

The current study evaluated the effects of triclopyr (3,5, 6-trichloro-2-pyridinyloxyacetic acid) on renal function following oral administration in the beagle dog and rhesus monkey. Male rhesus monkeys were orally administered triclopyr by gavage at a dose of 5 mg/kg/day, 7 days/week for 28 days, after which the dosage was increased to 20 mg/kg/day for 102 consecutive days. Groups of male dogs were administered either a single oral dose of 5 mg/kg triclopyr or were fed a diet spiked with triclopyr at a dose of 5 mg/kg/day for 47 consecutive days. The following functional and clinical chemistry parameters were evaluated: exogenous phenolsulfonphthalein (PSP) excretion, inulin and para-aminohippurate (PAH) clearance (monkeys only), endogenous serum creatinine, and blood urea nitrogen (BUN) at multiple time points during the study. Creatinine, BUN, and inulin clearance were within the normal range from both species following triclopyr administration which indicates that repeated administration of triclopyr in the dog and monkey had no effect on glomerular filtration rate (GFR). In monkeys, the percentage excretion of PSP and PAH appeared to increase following triclopyr administration (20 mg/kg/day), suggesting that these weak organic acids may be competing for the same plasma protein-binding site enhancing their clearance. More importantly, these data strongly suggest that triclopyr is not competing with PSP or PAH for the active secretory site within the monkey kidney proximal tubules. In contrast, PSP clearance studies in dogs clearly demonstrated that triclopyr administration (5 mg/kg) can significantly decrease the percentage PSP excretion even following a single dose administration. The decrease in percentage PSP was reversible and inversely related to the plasma triclopyr concentration. Overall, these data clearly indicate that triclopyr effectively competes with PSP for the active secretory site within the dog kidney proximal tubules. In contrast, the monkey was insensitive to the effects of triclopyr on the active secretory process even at doses fourfold higher (20 mg/kg/day) than the effective dose in the dog (5 mg/kg/day). These findings suggest that the effect observed on PSP and PAH excretion in the dog represent a physiological competition for excretion and not toxicity.

Administration, Oral↗
PubMed1984

Zinc, copper, manganese and iron in rat organs after the administration and withdrawal of aflatoxin B1.

The in vivo levels of zinc, copper, manganese and iron were determined in the testis, kidney and three brain regions (cerebellum, cerebrum and medulla oblongata) from rats intraperitoneally injected with 20 micrograms per kg body weight of aflatoxin B1 for 6 weeks. Similar investigations were made after a recovery period of 6 weeks. The results obtained were compared with those of pair-fed control rats. The aflatoxin B1-induced decrease in testicular zinc was not reversed after the recovery of the rats. On the contrary, the significantly increased zinc concentration in the other organs following aflatoxin B1 exposure, reverted to the control level, as judged by significant levels. Only in the kidney was there accumulation of copper, even after the cessation of aflatoxin B1 administration. The marked increase in the manganese concentration of all the organs following repeated toxin administration, persisted only in the brain regions after the recovery. Aflatoxin B1 treatment significantly decreased the iron concentration in the testis, kidney, cerebellum and cerebrum. Recovery did not alter this trend. Iron concentration in the medulla oblongata was, however, not significantly changed in the presence of aflatoxin B1. The present data suggest that the repeated administration of aflatoxin B1 to rats could result in either a permanent or temporary re-distribution of these elements in the organs examined.

Aflatoxin B1↗