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PubMed2000

The effect of lead on the eruption rates of incisor teeth in rats.

The effects of lead on the continuously erupting rat incisors under normo-, hyper- and hypofunctional conditions were investigated. Left lower incisors of 20 rats were rendered unimpeded (hypofunctional) by cutting them out of occlusion every 2 days; the right lower incisors of these rats were considered hyperfunctional. Measurements on normally growing teeth (normofunctional) were carried out in a group of ten rats whose teeth were not cut but only marked every 2 days. On day 7 of the experiment, half of the rats from these two groups were given a single intraperitoneal injection of lead acetate (40 mg/kg), and the other half received sodium acetate (22 mg/kg). Another group of 15 rats was used to obtain blood samples for lead determination 1 h, and 10, 20, and 30 days after lead administration. Animals were killed on day 32. Hypofunctional incisors from lead-treated rats erupted more slowly than control ones (P<0.05). These results show a previously unreported toxic effect of heavy metals.

Animals↗
PubMed1975

[Morphological effects of intraperitoneal oily fatty acids on the intestine and peritoneum of rats].

UNLABELLED: Changes of the mucosa of the small intestine in animal experiments can be produced by a variety of methods. The direct application of numerous chemical agents on the epithelium of the mucosa and parenteral administration of cytostatics as well as an indirect damage by experimental intestinal lymphatic obstruction lead to mucosal lesions with atrophy of the villi. Our paper presents a simple indirect method for induction of structural mucosa changes in rats using experimentally produced peritoneal alterations as a precursor. MATERIALS AND METHODS: The first experimental group with 108 male wistar rats was divided into 5 subgroups and treated as follows: 43 rats got continuous daily intraperitoneal injections of 3-3 ml/kg body weight sesame oil DAB 6 which contains 50% oleic acid, 36% linolic acid, 1% free fatty acids, 0.1% lecithin and portions of stearic, palmitic and arachic acid; 6 rats got 6.6 ml sesame oil per kg i.p., 43 animals received daily doses of 3-3 ml oil/kg per orally by a pharyngeal tube, 6 rats of each group were sacrificed after 68 and 92 days, all the rest were killed after 100 days of continuous daily treatment. Aortic blood was used for determination of the total cholesterol serum concentration. Blocks of tissue of every organ were fixed in 4% formalin, sections were stained with hematoxylin and eosin, hematoxylin-sudan and by the periodic acid Schiff (PAS-) method. For the purpose of autoradiographic determination of the 3H-thymidine labelling index the rats were administered i.p. 2 mCi 3H-thymidine/kg 40 minutes prior to death. Autoradiographs were prepared from sections of the small intestine by using liquid photoemulsion Ilford K5. In the second experimental group 7 rats got a single i.p. injection of 5 ml, 5 rats of the 10 ml and 9 rats of 20 ml sesame oil per animal; 4 rats were administered 8 ml daily for 5 days...

Animals↗
PubMed1998

Biochemical and connective tissue changes in cyclophosphamide-induced lung fibrosis in rats.

The present investigation was designed to characterize the biochemical and connective tissue components and to correlate the significance of morphological and biochemical perturbations in cyclophosphamide (CP)-induced lung fibrosis in rats. Lung fibrosis was induced in male Wistar rats by intraperitoneal injection of 20 mg/100 g body weight of CP, and their pneumotoxic derangements were characterized during an early destructive phase followed by a proliferative and synthetic phase. Serum angiotensin-converting enzyme (ACE) activity was higher in CP-treated rats at days 2, 3, 5, 7, and 11, but there was a significant decrease in lung ACE activity during the same time period. Elevated levels of beta-glucuronidase activity were observed in the lung lavage fluid of CP-administered rats days 2, 3, 5, and 7. Lung myeloperoxidase activity was higher in CP rats. Of significance was the presence of collagenase and collagenolytic cathepsin in the lavage fluid of CP rats, when compared with the barely detectable levels in controls. A similar increase in these enzyme activities was also noticed in the lung tissue of CP rats during the same experimental period. Lavage fluid hydroxyproline content was higher in CP rats when compared with controls. Similarly, lung protein and DNA levels were elevated significantly after treatment with CP. The pulmonary histamine and serotonin contents were significantly higher in CP rats. The incorporation of [3H]thymidine into lung total DNA, [3H]proline into lung hydroxyproline, and [35S]sulphate into lung glycosaminoglycan, measured as indicators of lung DNA, collagen, and glycosaminoglycan synthesis, respectively, was also higher in CP groups. Increased levels of hydroxyproline, elastin, hexosamine, total hexose, fucose, sialic acid, and uronic acid in the lungs of rats 14, 28, and 42 days after CP insult were characterized as biomarkers of CP-induced interstitial changes. These findings indicate that CP-induced lung fibrosis results in alterations not only in collagen synthesis and accumulation, but also in glycosaminoglycan and glycoprotein content.

Animals↗
PubMed2001

The area postrema lesions alter the inhibitory effects of peripherally infused pancreatic polypeptide on pancreatic secretion.

Circulating PP binds to specific receptors in the DVC through the AP, but the mechanism through which these brain receptors affect pancreatic secretion is not clear. We hypothesize that the removal of the AP (APX) will alter the effects of PP on pancreatic secretion. APX or sham procedures were performed in anesthetized male Wistar rats. After a 1-month recovery, one group of rats were infused with either PP (30 or 100 pmol/kg per h) or vehicle under basal or 2-DG-stimulated (75 mg/kg, i.v. bolus) conditions for studying pancreatic exocrine secretion. A second parallel group was sacrificed for examination of PP receptor binding in the brain stem. A third group received an intraperitoneal injection of PP at the dose of 4.15x10(4) pmol/kg (200 microg/kg) and c-fos expression in the brain stem was examined. APX eliminated PP binding sites in the DVC as assessed by autoradiography. PP infusion caused a dose-dependent decrease in basal protein secretion. APX partially reversed PP inhibition of basal protein secretion when infused at 30 pmol/kg per h, and at 100 pmol/kg per h stimulated pancreatic fluid secretion and reversed the inhibition of protein secretion. During 2-DG stimulation the effects of PP and 2-DG on pancreatic fluid and protein secretion were parallel. PP dose-dependently inhibited 2-DG-stimulated secretion in sham rats. APX reduced the pancreatic fluid (54%) and protein (46%) secretory response to 2-DG. However, PP at 30 pmol/kg per h remained a potent inhibitor of 2-DG-stimulated pancreatic secretion in APX rats. This effect was blunted with PP at 100 pmol/kg per h in APX rats, possibly related to the stimulatory effect of high-dose PP in APX rats without 2-DG. Furthermore, i.p. PP induced significantly greater c-fos activation of NTS neurons in APX rats than sham rats, despite the apparent absence of PP binding sites in the DVC. We conclude that in awake rats, PP inhibits basal secretion, in part, through the AP. Furthermore, and unlike PYY, PP inhibits 2-DG-stimulated pancreatic secretion, and it does so through an AP-independent mechanism. The possibility that the mechanism may involve the DVC cannot be excluded since i.p. injection of PP activates c-fos expression in DVC neurons. Thus, PP and PYY may regulate different components of the pancreatic secretory control system through unique pathways.

Animals↗
PubMed2001

Leukemia inhibitory factor by systemic administration rescues spinal motor neurons in the SOD1 G93A murine model of familial amyotrophic lateral sclerosis.

Leukemia inhibitory factor (LIF) is a survival factor for motoneurons. In this study we investigated whether intense systemic LIF therapy prevents the loss of lumbar motoneurons in the transgenic SOD1 G93A mouse model of familial amyotrophic lateral sclerosis. Treatment involved daily 25 microg/kg intraperitoneal injection for a period of 6 weeks starting at 70 days of age. Using the unbiased optical dissector technique, significant rescue of motoneurons in the LIF-treated group (3809+/-455) was found compared to the vehicle group (1085+/-140).

Amyotrophic Lateral Sclerosis↗
PubMed2003

Behavioural and anatomical effects of systemically administered leukemia inhibitory factor in the SOD1(G93A G1H) mouse model of familial amyotrophic lateral sclerosis.

We investigated the anatomical and behavioural effects of daily intraperitoneal injection of 25 microg/kg of LIF in the SOD1(G93A G1H) mouse model of familial ALS. We found some subtle beneficial behavioural changes in LIF treated mice. These included later onset of clinical disease in females as determined by clinical scoring; better grip strength in males; and delayed development of motor impairment in males as determined by the rotarod test. However, we found no significant rescue of motoneurons or prolongation of survival as a result of this systemic dose of LIF in these mice.

Aging↗
PubMed1997

Effects of thymosin alpha1 on the development of amoeboid microglial cells in the corpus callosum of neonatal BALB/c and athymic mice.

The present study investigated the effects of intraperitoneal injections of thymosin alpha1 on the supraventricular amoeboid microglial cells (SAMC) in the newborn athymic and normal BALB/c mice. The microglial cells labelled by the lectin GSA I-B4 and the antibody Mac-1 showed a 27% reduction in number in the athymic mice receiving thymosin alpha1 injections compared with those receiving vehicle injections, and a 37% reduction in BALB/c mice receiving thymosin alpha1 injections compared with those receiving vehicle injections. Some of the SAMC in both BALB/c and athymic mice receiving thymosin alpha1 injections became ramified, while the remainder still exhibited their normal amoeboid appearance with few filopodial processes. Ultrastructurally, the lectin reaction product was confined to the plasma membrane and some cytoplasmic vacuoles of labelled SAMC. In both BALB/c and athymic mice, some labelled microglial cells became slender or elongated after thymosin alpha1 injections. Also their cytoplasm was reduced and contained fewer organelles. Radioimmunoassay of the plasma of thymosin alpha1 and vehicle-injected mice showed that there was a significant increase in the cortisol level in BALB/c (P < 0.01) and athymic (P < 0.001) mice 5 days after thymosin alpha1 injections, compared with that of the control mice. The results point to a strong correlation between the reduction of SAMC and the increased level of plasma cortisol. Supporting this is the fact that cortisol is known to suppress the production of monocytes considered to be the precursors of amoeboid microglia.

Adjuvants, Immunologic↗
PubMed1997

Ethanol-induced c-Fos expression in rat lines selected for low and high alcohol consumption.

Selectively bred rat lines, developed to model genetic contributions to alcohol abuse, include the Indiana alcohol-preferring (P) and alcohol-nonpreferring (NP) lines, and the Alko-Alcohol (AA) and Alko-Nonalcohol (ANA) lines. Preferring and nonpreferring lines were compared in their response to intraperitoneal injection of either ethanol or isotonic saline using c-Fos expression as a marker of neuronal activity. Although line differences were noted in several brain regions, the principal finding was that alcohol-nonpreferring lines (NP and ANA) displayed greater c-Fos expression in the locus coeruleus (LC) relative to the alcohol-preferring lines (P and AA) following injection of 3.0 g ethanol/kg. These data point to the LC as an area which may play a role in the differences in voluntary ethanol consumption between rat lines genetically bred for low and high ethanol preference.

Alcohol Drinking↗
PubMed1997

The antidopaminergic action of S-20098 is mediated by benzodiazepine/GABA(A) receptors in the striatum.

The naphthalenic compound S-20098, which is a melatonergic agonist, inhibits [3H]diazepam binding in striatal membranes. S-20098 also inhibits apomorphine-induced turning in 6-hydroxydopamine lesioned rats. This antidopaminergic effect is blocked by either intraperitoneal injection of the central-type benzodiazepine (BZ) antagonist, flumazenil, or intrastriatal injection of the GABA(A) antagonist, bicuculline. These findings indicate that S-20098 can activate central-type BZ receptors, and its antidopaminergic action, like that of melatonin, involves a GABAergic mechanism in the striatum.

Acetamides↗
PubMed1998

Effect of macrophage suppression with silica on the proliferation of Schwann cells during Wallerian degeneration.

Effects of macrophage suppression on Schwann cell proliferation in Wallerian degeneration was investigated in vitro with thymidine autoradiography. Sciatic nerves of C57BL mice were transected shortly after an intraperitoneal injection of silica dust and Schwann cells were harvested at 1, 2, 3, 5, 7, and 10 days post-transection. In silica treated mice, Schwann cells from post-transected nerve stumps proliferated despite marked suppression of macrophages, although there was some initial delay. The results of this study suggest that the mechanism of Schwann cell proliferation is multifactorial and in addition to the influence of growth factors mediated and released by macrophages, other factor(s) such as degenerated axolemma may play a more pivotal role in Schwann cell proliferation in vivo.

Animals↗
PubMed1999

Regional expressions of Fos-like immunoreactivity in rat cerebral cortex after stress; restraint and intraperitoneal lipopolysaccharide.

To demonstrate regional activation in the rat cerebral cortex related to stress-evoked neuroendocrine response, Fos expression in both the cerebral cortex and hypothalamic paraventricular nucleus (PVN) was immunohistochemically examined in two experimental groups; a lipopolysaccharide (LPS) intraperitoneally injected group for inflammatory stress and a restraint group for emotional stress. The LPS injection (100 microg/100 g b.w.) and restraint (for 30 min) had similar effect on Fos-like immunoreactivity (Fos-LI) in PVN with regard to the number of immunoreactive nuclei and their distribution pattern, while the times to maximize Fos-LI were different. Numerical analysis of cortical Fos-LI in untreated rats showed a distinct region-specific pattern. Statistical analysis revealed no significant increase in Fos-LI density in any cortical regions in the LPS group, but restraint resulted in a dramatic and region-specific increase. A significant increase was detected in the prefrontal cortex (the cingulate, orbital and agranular insular cortex), the frontal area 2, the agranular retrosplenial cortex, the parietal cortex, and the medial and lateral occipital area 2. These results indicate that cortical activation relevant to specific functions may be involved in stress-specific neural circuitry.

Animals↗
PubMed2001

Protective effect of various antioxidants on the toxicity of sulphur mustard administered to mice by inhalation or percutaneous routes.

Protective effect of various antioxidants, trolox (water soluble analogue of vitamin E), quercetin (bioflavonoid) and glutathione reduced (GSH), was studied following sulphur mustard (SM) intoxication. SM, a blistering agent was administered to Swiss albino female mice through inhalation (1 LC50=42.3 mg/m3 for 1 h duration; 14 days observation for mortality) and percutaneous (1 LD50=154.7 mg/kg; 7 days observation for mortality) routes. The antioxidants were administered three times at the dose of trolox, 500 microg/kg; quercetin, 5 mg/kg and GSH, 400 mg/kg body weight by intraperitoneal injection, one immediately following SM exposure, then once each day for 2 days after SM treatment. The effect of antioxidants on survival, markers of oxidative damage and purine metabolites was investigated. Survival study animals were observed for 14 days. Oxidative markers (in blood, liver and lung) and purine metabolites (in blood and urine) were investigated 72 h after SM treatment. Survival time increased significantly following trolox and quercetin treatments through the inhalation route. Significant decrease in GSH and increase in the level of malondialdehyde (MDA) indicated oxidative damage to liver and lung tissues following SM inhalation and percutaneous exposure. Blood and urinary uric acid, end product of purine metabolism showed an increased following both routes of exposures. The antioxidants, trolox and quercetin protected the liver and lung tissues from oxidative damage caused by SM exposure through inhalation and percutaneous routes. This study showed that antioxidants could enhance survival time, protect liver and lung from oxidative damage and reduce accumulation of purine metabolites in blood following SM intoxication.

Administration, Cutaneous↗
PubMed1990

Uptake of mercury by the hair of methylmercury-treated newborn mice.

Human hair has unique advantages in monitoring environmental exposures to methylmercury. Using newborn Balb/c mice as a model system, the incorporation of methylmercury into the hair was studied and compared with methylmercury distributions in other tissues. Newborn mice were given intraperitoneal injections of 203Hg-labeled methylmercury at designated times according to hair growth stages of the mouse. Animals were sacrificed 2 days after dosing. Distribution of mercury in pelt and other tissues was measured. The level of mercury in pelt was found to correlate with hair growth. The amount of mercury in pelt peaked when hair growth was most rapid and the total amount of mercury in pelt was significantly higher than that in other tissues, constituting 40% of the whole body burden. However, when the hair ceased growing, the amount of mercury in pelt dramatically dropped to 4% of whole body burden and mercury concentrations in other tissues except brain were elevated. Autoradiographic studies with tritium-labeled methylmercury demonstrated that methylmercury concentrated in hair follicles in the skin. Within hair follicles and hairs, methylmercury accumulated in regions that are rich in high-sulfur proteins. The uptake of inorganic mercury (administered as HgCl2) by pelt was also compared with that of methylmercury. The amount of inorganic mercury found in pelt was less than one-half that of methylmercury in animals with growing hair. Cessation of hair growth did not decrease the inorganic mercury level in pelt to the same extent as in the case of methylmercury.

Animals↗
PubMed1991

Mercury in the dorsal root ganglia of rats treated with inorganic or organic mercury.

Autometallographic silver amplification has been used to demonstrate the localization of mercury deposits in rat dorsal root ganglia after repeated intraperitoneal injections of mercuric chloride or methylmercuric chloride. The silver-enhanced mercury deposits were demonstrated with the light and electron microscope. The degree of intracellular staining of the individual cells depended on the mercury compound and total dosage. Ganglion cells (types A and B) and macrophages were found to accumulate mercury after a total dosage of 400 micrograms HgCl2. After 600 micrograms HgCl2, satellite cells, endothelial cells and fibroblasts were additionally found to contain mercury deposits. Treatment with 6000 micrograms CH3HgCl caused faint staining of type A and B ganglion cells and fibroblasts. Macrophages, however, were the most heavily stained cells after treatment with CH3HgCl. Ultrastructurally, mercury was exclusively located in lysosomes. This was irrespective of the cell type and mercury compound used for treatment.

Animals↗
PubMed1986

Concentration and chemical status of arsenic in the blood of pregnant hamsters during critical embryogenesis. 2. Acute exposure.

We have determined the concentration and chemical composition of arsenic in the blood of pregnant hamsters between 0.2 and 6 hr after an intraperitoneal injection of a teratogenic dose of radiolabeled sodium arsenate on the morning of the eighth day of gestation. Arsenic was present in plasma and red cells 0.20 hr postinjection. The plasma arsenic concentration reached a maximum of 220 mumole/kg blood near 0.5 hr postinjection. Plasma arsenic existed entirely as low-molecular-weight species. Both arsenite and dimethylarsinate (DMA) were present in plasma 0.20 hr postinjection, indicating that arsenate reduction and methylation of arsenic are rapidly initiated. However, the arsenite contribution remained small while the DMA contribution increased with time. Red cell arsenic included macromolecular arsenic (AsP) as well as three low-molecular-weight forms. The contribution of DMA remained small, but arsenite and AsP contributions increased with time. These findings identify the maternal blood concentration and chemical status of arsenic following the administration of a teratogenic dose of arsenate during the period of organogenesis. They could prove useful for predicting the likelihood of a teratogenic outcome in other mammalian species.

Animals↗
PubMed1986

Dose-dependent metabolism of trichloroethylene and its relevance to hepatotoxicity in rats.

Fasted male Sprague-Dawley rats pretreated with phenobarbital received an intraperitoneal injection of 0.00, 0.25, 0.50, 0.75, 1.00, 1.50, or 2.00 ml/kg of trichloroethylene (TRI) in corn oil. The metabolic fate of TRI was monitored by measuring its major urinary metabolites 24 hr following the dosing. The hepatotoxic response of TRI was evaluated by determination of the serum transaminase activities (SGOT and SGPT) 24 hr after dosing. Treatment of rats with TRI up to 0.5 ml/kg did not affect the transaminase responses, but significant response was manifested at 0.75 ml/kg dose. Further continuous increases in such responses were induced on exposure to higher doses. Dose-dependent urinary excretions of trichloroethanol and trichloroacetic acid were observed and reached an apparent saturation at 1-1.5 ml/kg dose of TRI. The percentage of dose excreted as trichloroethanol was decreased from 16% at 0.25 ml or 2.8 mmole/kg to 8% at 2 ml or 22.3 mmole/kg dose. The percentage of trichloroacetic acid was decreased from 5 to 2% for the same dose interval. A maximum of only 29% depletion of hepatic glutathione was observed at 2 hr following 1 ml/kg dose of TRI. Similarly, the excretion of urinary mercapturic acid of TRI or thioether was insignificant at any dose level. These results suggest that the conjugation of hepatic glutathione with the electrophilic intermediate of TRI does not seem to be an important determinant for TRI hepatotoxicity nor the major detoxification pathway of its reactive intermediate. TRI produced also a dose-dependent decrease in hepatic microsomal monooxygenase activities as well as cytochrome P-450 content. All these results, when combined, show that there exists an apparent saturable metabolism of TRI involving its activation/deactivation pathways which correspond to an apparent threshold or minimal toxic dose, about 1 ml/kg or 11.15 mmole/kg of TRI for its hepatotoxicity.

Aminopyrine N-Demethylase↗
PubMed1986

Acute toxicity of Microcystis aeruginosa and its cardiovascular effects.

The acute toxicity of a water extract from unialgal-cultured blue-green alga Microcystis aeruginosa M228 on mice and rats was studied. The mice intraperitoneally injected with the extract became lethargic and piloerection was seen. Terminally their ears, tails, limbs, and eyes became chalky white. The LD50 value of the extract for mice was estimated at 14.4 mg dry wt of cells/kg and that of rats was 67.4 mg/kg. Tachycardia was shown in the mice injected with the extract. A value of LD50 of coadministration of the extract and phenoxybenzamine in mice was significantly larger than that of the extract alone and survival time of mice injected with the extract and phenoxybenzamine was prolonged. These results suggest that the extract of the alga may take the acute toxic effects via the sympathetic nervous system.

Animals↗
PubMed1988

Fluorocarbon-enhanced mutagenesis of polyaromatic hydrocarbons.

The widely used fluorocarbon refrigerant and cleaning solvent 1,1,2-trichloro-1,2,2-trifluoroethane (Freon TF), though generally considered biologically inert, enhances the metabolic activation of chemical carcinogens. Liver microsomal extracts from mice given single intraperitoneal injections of this fluorocarbon showed significant increases in their ability to activate carcinogenic polyaromatic hydrocarbons to form mutagens, compared to control mice injected with saline. Polyaromatic hydrocarbons aminofluorene and acetylaminofluorene were activated in this way. Mutagenicity was measured by a microbial assay. Both commercial grade and redistilled fluorocarbons gave similar results, that is, more highly active liver extracts after administration of the fluorocarbon preparation to mice. Neither industrial grade nor redistilled preparation was itself mutagenic. A combined liver microsomal extract from mice breathing Freon TF at 20,000 ppm in air for 8 hr also had enhanced ability to activate aminofluorene as a mutagen. Exposing mice to Freon TF by inhalation more closely matches the normal route of human exposure to fluorocarbons. The results of this study imply that low-molecular-weight fluorocarbons may pose a carcinogenic risk by acting as cocarcinogenic enhancers of carcinogen activation. The possibility that fluorocarbons are cocarcinogens in this way has apparently not been heretofore considered.

Administration, Inhalation↗