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PubMedDate not supplied

Neuroleptic-like properties of cholecystokinin analogs: distinctive mechanisms underlying similar behavioral profiles depending on the route of administration.

Rats were trained to discriminate vehicle injections from intraperitoneal injections of 3 micrograms/kg caerulein, a cholecystokinin (CCK) neuropeptide analog. The reward that reinforced correct choices was an electrical brain stimulation self-administered by bar pressing. Dose-response quantitative generalization was obtained by using 1 and 2 micrograms/kg caerulein. Qualitative generalization to the vehicle occurred after injecting 10, 20 and 200 micrograms/kg unsulfated CCK-8, 10, 20 and 200 micrograms/kg CCK-4, 5 micrograms/kg CCK-8 and 1 microgram/kg caerulein, neurotensin or bombesin and 200 micrograms/kg apomorphine or 320 micrograms/kg amphetamine. Total generalization to the caerulein cue was obtained with 20 micrograms/kg sulfated CCK-8 or gastrin 2-17, 25 micrograms/kg somatostatin, 50 micrograms/kg haloperidol and 2 mg/kg chlorpromazine. The previous 5 mg/kg injection of an antiemetic drug such as chlorhydrate of trimethobenzamide did not eliminate the discriminative properties of a subsequent injection of caerulein. Our data thus tend to show that IP injection of caerulein produces effects similar to those of IP neuroleptics.

Animals↗
PubMed1994

Rapid and selective enhancement of DNA binding activity of the transcription factor AP1 by systemic administration of N-methyl-D-aspartate in murine hippocampus.

Brain nuclear extracts of ddY mice contained 3 different transcription factors with leucine-zipper domains, including activator protein-1 (AP1), cyclic AMP responsive element binding protein (CREB) and Myc. An intraperitoneal injection of N-methyl-D-aspartate (NMDA) was effective in selectively inducing 6-fold enhancement of DNA binding activity of AP1 in the hippocampus 2 h after the administration. Furthermore, NMDA induced less than 2-fold potentiation of the AP1 binding in the striatum, hypothalamus, medulla-pons and cerebral cortex in a rank order of decreasing magnitude. However, the AP1 binding was not significantly affected by the systemic injection of NMDA in the midbrain and cerebellum. In contrast, NMDA virtually did not alter DNA binding activities of both CREB and Myc in discrete structures of murine brain under similar experimental conditions. These results suggest that the systemic administration of NMDA may induce rapid and selective enhancement of DNA binding activity of AP1 in murine hippocampus.

Animals↗
PubMedDate not supplied

Influence of aging on the acute depletion of reduced glutathione induced by electrophilic agents.

A severe age-dependent depletion of reduced glutathione (GSH) occurs in rat forebrain at 1-3 h from intraperitoneal injection of the electrophilic agents cyclohexene-1-one and cycloheptene-1-one. Chronic pretreatment with central dopamine agonists (i.e., ergot alkaloids; particularly, dihydroergocriptine) partially counteracts the GSH depletion induced in 15-month-old forebrains by the prooxidants tested. In contrast, chronic pretreatment with a vasodilator agent (i.e., papaverine) magnifies the GSH depletion.

Aging↗
PubMed1986

Acute toxicity studies with oxamyl.

The acute toxicity of oxamyl, an insecticide and nematicide, has been evaluated to establish proper handling guides. The material is highly toxic when given as a single oral dose; its LD50 is in fasted rats 2.5 to 3.1 mg/kg, 2.3 to 3.3 mg/kg in fasted mice, and 7 mg/kg in guinea pigs. A beagle dog given 30 mg/kg died, while 15 mg/kg was not lethal. In all species, clinical signs of cholinesterase inhibition (lacrimation, salivation, tremors) were observed. Cholinesterase activity was depressed in rats treated with a single oral dose. Atropine, when given immediately after oxamyl, was antidotal. When given by intraperitoneal injection, oxamyl was highly toxic to rats, mice, and guinea pigs. The material is a mild eye irritant with the reaction limited to the conjunctiva and iris, but systemic absorption via eye contact makes use of protective equipment essential. Oxamyl produces mild skin irritation and the dermal absorption toxicity in rats (LD50 is greater than 1,200 mg/kg) and rabbits (740 mg/kg) is relatively high suggesting limited absorption. No sensitization was produced when tested in guinea pigs. Oxamyl is highly toxic via inhalation with the 1-hr LC50 value in rats being 0.17 mg/liter (male) and 0.12 mg/liter (female). The corresponding 4-hr value is 0.064 mg/liter for male rats which indicates that concentration X time is a constant through the time periods tested. Repeated-dose studies, orally in rats and dermally in rabbits, showed oxamyl to be noncumulative, with the target system being the nervous system mediated through cholinesterase inhibition. No specific tissue or organ pathology was seen in either species tested.

Administration, Oral↗
PubMed1982

Whole-body autoradiography of 204Tl in embryos, fetuses and placentas of mice.

Whole-body autoradiography was used to study thallium uptake and retention in mice during gestation. Fifteen minutes after an intraperitoneal injection of 50 microCi 204Tl2SO4 into a 15-day pregnant mouse, thallium could be seen within the fetuses. Maximum fetal accumulation occurred 2-4 h after injection, and minimum at the last observation 4 days after injection. The fetal concentration of 204Tl was constantly lower than the placental. Uptake of 204Tl in embryos, fetuses and placentas of mice with gestation ages varying from 5 days to 16 days indicated that thallium crosses the placental barriers throughout gestation. Thallium was retained by the visceral yolk sac placenta during early gestation, by the visceral yolk sac, chorioallantoic placenta and amnion during late gestation. Over a period of time placental transfer and embryonic/fetal retention of small amounts of thallium may be hazardous to the offspring due to the high cumulative toxicity of this metal.

Animals↗
PubMed1984

The selective action of nickel on tubule function in rabbit kidneys.

Two days after intraperitoneal injection of NiCl2 (20 mumol/kg) into rabbits the same apparently uncompetitive inhibition of aspartate reabsorption is seen as was previously observed following acute exposure to other metals. This dose of Ni reduced the calculated maximum tubular transport rate for aspartate (Tm) and the apparent affinity constant (KM) by over 50%, but exerted no effect on either Tm or KM of cycloleucine or glucose reabsorption. The relative selectivity of the nephrotoxic action of Ni and other metals is reviewed; it raises the question whether the acute effects observed are appropriately described as a Fanconi-like syndrome.

Absorption↗
PubMed1987

Silver-induced lipid peroxidation in mice: interactions with selenium and nickel.

Lipid peroxidation in silver-treated mice was assayed by measuring the malondialdehyde (MDA) content of liver, kidney and brain tissue. After a single intraperitoneal injection of 20 mg/kg silver lactate, lipid peroxidation was significantly increased in the liver 3, 12 and 48 h after exposure whereas MDA levels in kidney and brain were not significantly affected. Pretreatment with 2 mg/kg sodium selenite i.p. for 2 days resulted in an increase in silver-induced lipid peroxidation in the liver. Liver from mice treated with 20 mg/kg silver lactate followed by an injection of 35 micrograms/kg nickel chloride had significantly higher contents of MDA than did livers from mice treated with either silver or nickel alone, suggesting a synergism between silver and other lipid peroxidation-inducing compounds.

Animals↗
PubMed1989

Formation of nuclear anomalies in rat intestine by benzidine and its biliary metabolites.

Administration of benzidine (BZ) by intraperitoneal injection (i.p.) to rats (0-100 mg/kg) produced, after 24 h, a dose-dependent formation of nuclear anomalies (micronuclei, pyknotic and karyorrhectic nuclei) in intestinal epithelial cells analysed both in isolated cell suspensions and in the intestinal crypts in tissue sections. When bile collected (0-4 h) from rats treated with BZ (150 mg/kg, i.p.) was infused into the duodenum of recipient rats, nuclear anomalies were observed in mucosal epithelial cells, after 24 h, with a similar distribution to that in rats given BZ by i.p. injection. The formation of nuclear anomalies in the intestine is in accord with the intestinal carcinogenic effect of BZ and is, at least partially, dependent on exposure of epithelial cells to biliary metabolites of BZ.

Animals↗
PubMed1992

Combined exposure to NO2, O3 and H2SO4-aerosol and lung tumor formation in rats.

The promoting effects of a combined exposure to two pollutants (NO2, O3 or H2SO4-aerosol) at near ambient levels on lung tumorigenesis induced by N-bis(2-hydroxypropyl) nitrosamine (BHPN) were investigated in male Wistar rats. The rats were given a single intraperitoneal injection of BHPN (0.5 g per kg body wt.) at 6 weeks of age. They then were exposed to clean air, 0.05 ppm O3 (mean concentration for 10 h/day; 0.1 ppm peak concentration), 0.05 ppm O3 (mean concentration for 10 h/day; 0.1 ppm peak concentration) + 0.4 ppm NO2 or 0.4 ppm NO2 + 1 mg/m3 of H2SO4-aerosol for 13 months and were then maintained in a clean room for another 11 months. Room control animals were kept after injection of BHPN in a clean room for 24 months. The incidence of primary lung tumors in rats exposed to 0.05 ppm O3, 0.05 ppm O3 + 0.4 ppm NO2 and 0.4 ppm NO2 + 1 mg/m3 of H2SO4-aerosol with BHPN treatment was 8.3% (3 out of 36 rats), 13.9% (5 out of 36 rats) and 8.3% (3 out of 36 rats), respectively. The tumors were adenomas and adenocarcinomas. The incidence of adenomas was 2.8% (1 out of 36 rats) in the O3 alone group, 11% (4 out of 36 rats) in O3 + NO2 group and 5.6% (2 out of 36 rats) in NO2 + H2SO4 group. The incidence of adenocarcinomas was 5.6% (2 out of 36 rats) in the O3 group, 2.8% (1 out of 36 rats) in O3 + NO2 group and 2.8% (1 out of 36 rats) in NO2 + H2SO4 group. No lung tumors were found in the rats exposed to clean air with BHPN treatment and in animals not given BHPN but exposed to each air pollutant. The difference in tumor incidence between the clean air group with BHPN and the O3 + NO2 group with BHPN was statistically significant. The results show that exposure to O3 alone enhances tumor development and that the combined exposure to O3 or H2SO4 with NO2 produces an additional increase in incidence of lung tumor, respectively. The incidence of slight-moderate to marked alveolar cell hyperplasia in the groups exposed to each air pollutant with BHPN treatment was higher than that in the groups exposed to clean air with BHPN. Exposure to each air pollutant had no effect on the development of bronchiolar mucosal hyperplasia in lungs of rats treated with BHPN.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗
PubMed1995

Demonstration of chlorobenzene-induced DNA damage in mouse lymphocytes using the single cell gel electrophoresis assay.

The DNA damaging effect of chlorobenzene was investigated in peripheral lymphocytes and bone marrow cells from C57BL/6 female mice using a gel electrophoresis assay for DNA from single cells ('the single cell gel electrophoresis assay') under alkaline conditions. The effect of chlorobenzene was studied both after single and repeated intraperitoneal injections of 750 mg/kg body weight. The cytostatic agent cyclophosphamide (150 mg/kg, i.p.) was used as a reference substance, and vehicle-treated mice as controls. DNA damage was recorded 16 h after the (last) injection, using an automated computerized image analysis system specifically designed for the single cell gel electrophoresis assay. There was evidence of chlorobenzene-induced DNA damage after 3 days of repeated exposure in peripheral lymphocytes, but no indications of such an effect in bone marrow cells. Cyclophosphamide induced significant damage to DNA both in bone marrow cells and lymphocytes, the effect being most pronounced in the latter cells. It is concluded that high-dose exposure to chlorobenzene is associated with genotoxicity to peripheral lymphocytes. However, this solvent is apparently not a major hazard to bone marrow cells, even after repeated high-dose exposure.

Analysis of Variance↗
PubMed1994

Comparative effects of chelating agents on distribution, excretion, and renal toxicity of gold sodium thiomalate in rats.

The effects of various chelating agents, such as (2S)-1-(3-mercaptopropionyl)-L-proline (captopril), N-(2-mercaptopropionyl)-glycine (tiopronin), L-cysteine (L-Cys), D-cysteine (D-Cys), N-acetyl-L-cysteine (L-NAC), N-benzyl-D-glucamine dithiocarbamate (BGD), and ethylenediaminetetraacetate (EDTA), on the distribution, excretion, and renal toxicity of gold sodium thiomalate (AuTM) in rats were investigated. Rats were intraperitoneally injected with the chelating agents (1.2 mmol/kg each) immediately after intravenous injection of AuTM (0.026 mmol/kg). Treatment with captopril or tiopronin significantly prevented increases in the urinary excretion of protein, aspartate aminotransferase (AST), and glucose and the blood urea nitrogen (BUN) level after AuTM injection. L-NAC and D-Cys significantly prevented increases in the urinary excretion of protein, AST, and glucose after AuTM injection, but did not reduce to control levels. Treatment with BGD, EDTA, or L-Cys did not prevent AuTM-induced increases in the urinary excretion of protein, AST, and glucose and BUN level. Tiopronin significantly increased the urinary excretion of gold. Captopril slightly promoted both the urinary and fecal excretion of gold, resulting in the significant increase in the total excretion of the metal. Tiopronin and captopril significantly decreased the gold concentration in the kidney and liver. L-Cys, D-Cys, L-NAC, BGD, and EDTA had no significant effect on the excretion or distribution of gold at 7 days after AuTM injection. These results indicate that tiopronin and captopril can ameliorate the renal toxicity induced by AuTM. In addition, the comparative effects of 2,3-dimercaptopropane sulfonate (DMPS), N-(2-mercapto-2-methylpropanoyl)-L-cysteine (bucillamine), captopril, and tiopronin at various dose levels (1.2, 0.4 or 0.2 mmol/kg) on the distribution and renal toxicity of gold were studied. DMPS was effective in removing gold from the kidney and in protecting against the renal toxicity after AuTM injection at the even lower dose level (0.2 mmol/kg). Bucillamine and tiopronin protected against the renal toxicity of gold at dose levels of 0.4 and 1.2 mmol/kg and captopril ameliorated the gold toxicity only at higher dose level (1.2 mmol/kg).

Animals↗
PubMed1996

HI-6 therapy and the acute phase response in the rat.

The propensity of therapeutic doses of HI-6 (50 mg/kg) in combination with atropine sulphate (17 mg/kg), antidotes used to treat organophosphate poisoning, to induce the acute phase response (APR) in the laboratory rat was examined. A single intraperitoneal injection of HI-6, either alone or with atropine, caused a rapid doubling of the plasma corticosterone concentration. However, this increase was short-lived in comparison with corticosterone kinetics during the typical, turpentine-induced APR. The elevated glucocorticosteroid concentration did not affect acute phase protein (APP) gene transcription or mRNA and protein synthesis in the livers of oxime/atropine-treated rats. On the basis of these findings, we concluded that the administered doses of HI-6 and atropine did not induce the generalised, non-specific APR.

Acute-Phase Proteins↗
PubMed1996

Sodium 2,3-dimercapto-1-propanesulfonate (DMPS) treatment does not redistribute lead or mercury to the brain of rat.

Since there has been concern about whether any of the chelating agents used therapeutically might cause an initial redistribution of heavy metals to the brain and since the sodium salt of 2,3-dimercapto-1-propanesulfonic acid (Dimaval, DMPS) has been used to treat heavy metal intoxication in humans, the hypothesis that DMPS does not redistribute and increase lead or mercuric ions in the brains of rats was tested. Lead acetate at a concentration of 50 mg/l was made available in the drinking water of rats for 86 days. Other rats received intraperitoneal injections of 0.50 mg Hg/kg (as mercuric chloride) each day for 5 days a week for a total of 32 or 41 days. Animals were divided into groups and given, i.p., either 0.27 mmol DMPS/kg body weight or saline, each day for 1, 2, 3 or 4 days. Lead or mercury concentrations of the brain were determined after each group received DMPS for the different number of days. DMPS treatment did not result in any initial increase of lead or mercuric ions in the brain. The mercury content of the kidney decreased. The results of these experiments demonstrated that lead or mercuric ions were not redistributed to or increased in the brains of rats during the initial days of DMPS treatment.

Administration, Oral↗
PubMed1984

Effect of 1,8-dihydroxy-9-anthrone (anthralin) on rat hepatic ornithine decarboxylase activity in vivo.

Intraperitoneal injection of the non-phorbol tumor promoter anthralin (1,8-dihydroxy-9-anthrone) in male rats resulted in an increase of hepatic ornithine decarboxylase (ODC) activity. Maximal activity was observed 8 h after promoter administration reaching levels about 30 times over control. The kinetics of anthralin dependent ODC induction differed markedly from that by either 12-O-tetradecanoylphorbol-13-acetate (TPA) or phenobarbital (PB) (Bisschop et al., Carcinogenesis 2 (1981) 1282). With anthralin a slow decrease of ODC back to control level is observed approximately within 22 h. In contrast, ODC induction mediated by other tumor promoters like TPA and PB decreased to control levels within 4-6 hours. Administration of a second dose of anthralin 8 h after the first dose prevented the activity decrease as normally observed after a single dose of a tumor promoter. This effect lasted at least 10 h. ODC activity induction occurred in a dose-dependent manner being linear from 10-2000 micrograms anthralin/kg body wt. Pretreatment of the animals either with actinomycin D or with cycloheximide completely blocked anthralin mediated ODC induction suggesting that de novo ODC-mRNA synthesis and subsequent translation is involved in this process.

Animals↗
PubMed1987

Distribution and metabolism of ellagic acid in the mouse following intraperitoneal administration.

The distribution and metabolism of ellagic acid (EA), a naturally occurring plant phenolic compound with reported antimutagenic and anticarcinogenic activity, was investigated in mice following intraperitoneal injection. Male Swiss-Webster mice were given a single i.p. injection of [3H]EA and sacrificed at 15 min, 30 min, 60 min, 120 min and 24 h post-injection. At these times urine, blood and bile samples were obtained from each animal and various organs were removed, weighed and homogenized. Radioactivity in the samples was determined at each time interval and expressed as nmol [3H] EA/mg sample. Metabolites in urine and bile were analyzed by high-performance liquid chromatography (HPLC) and water-soluble conjugates were isolated by eluting samples of urine and bile from an alumina column. Radioactivity expressed as nmol [3H] EA/mg sample (wet weight) decreased with time in most organ homogenates. The peak radioactivity in bile appeared at 60 min post-injection while the peak radioactivity in urine occurred at 120 min. The two organs showing the highest amount of radioactivity were kidney and liver and the lowest was in brain. HPLC analysis revealed one unidentified metabolite of EA in bile and three in urine. Most of the radioactivity recovered from both bile and urine was associated with EA. Water-soluble conjugates in urine were isolated as sulfate esters, glucuronide and glutathione conjugates. Water-soluble conjugates in bile were evenly distributed as glucuronide and glutathione conjugates.

Animals↗
PubMed1992

Antitumor activity of phytic acid (inositol hexaphosphate) in murine transplanted and metastatic fibrosarcoma, a pilot study.

We have previously reported that phytic acid (inositol hexaphosphate or InsP6), a natural constituent of cereal diet, when administered in drinking water exerts a consistent antitumor effect on experimental colon cancer in vivo. The objective of this study was to determine whether InsP6 has similar anti-neoplastic effect on other tumor models, such as murine fibrosarcoma. We report that intraperitoneal injection of InsP6 reduces growth of subcutaneously transplanted fibrosarcoma (FSA-1) in mice, prolongs survival of tumor-bearing mice and reduces the number of pulmonary metastases. Since InsP6 is a common constituent of our diet and has very little or no toxic effects, in addition to being chemopreventive, it could have potential use in therapy of cancer as well.

Animals↗
PubMed1994

Effect of route of administration of environmental methylating agents on 7-methylguanine formation in white blood cells and internal organs: implications for molecular epidemiology.

The measurement of 7-methylguanine (7-meG) in white blood cells (WBC) is a promising biomarker of individual human exposure to environmental methylating agents. To test the validity of using WBC as a surrogate dosimeter for internal tissues, levels of 7-meG were measured in rat WBC, liver and target organs for carcinogenesis 16 h after oral administration of several methylating carcinogens (DMN, DMH, NNK, NMBA). 7-MeG was detected in WBC DNA but levels were far lower than in internal organs. While the ratio between 7-meG formation in target organs and WBC was highly variable depending on the carcinogen administered, the ratio between 7-meG in the liver and WBC was in the same order of magnitude for each carcinogen, ranging from 81 to 143. In addition, levels of 7-meG in the liver and WBC within individual animals were highly correlated (r = 0.94, P < 0.0001). These results confirmed our previous observations with the same carcinogens after intraperitoneal injection. In order to assess if the lower level of 7-meG in WBC was a result of a low metabolism of methylating agents in WBC, microsomes were prepared from control rat lymphocytes and DMN demethylase activity was measured. The total amount of microsomal proteins was extremely low, especially in comparison with hepatic cells, and the enzymatic activity was less than 0.48 nmol HCHO/min/mg protein, while an activity of 1.26 nmol HCHO/min/mg protein was measured in liver microsomes. Taken together, these results suggest that the presence of 7-meG in WBC DNA reflects an exposure to methylating agents; the level of 7-meG in WBC seems predictive of the level of adduct in the liver, possibly because active methylating species are formed in the liver and then transferred into the hepatic circulation, where the WBC are exposed. It is now important to examine this relationship in humans where exposures are generally to lower levels of carcinogens over long time periods.

Administration, Oral↗
PubMed1985

Sleep-promoting effects of intraperitoneally administered uridine in unrestrained rats.

An intraperitoneal injection of 0.1 nmol uridine in rats resulted in a transient excess slow-wave sleep if administered shortly before onset of the dark period. The sleep latency was remarkably shortened. A small dose (0.01 nmol) and larger doses (1, 10, 100 nmol) caused no effect. Uridine at a dose of 0.1 nmol was entirely ineffective if injected shortly before onset of the light period, while it resulted in transient excess paradoxical sleep if injected at an early phase of the light period. It is concluded that uridine, if timely administered through a systemic route, may pass the blood-brain barrier to modulate sleep in rats.

Animals↗