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PubMed1994

Ultrastructure of mice Leydig cells at chronic lead intoxication.

In the present paper we report on the study of the ultrastructure of Leydig cells of male mice after application of various doses of Pb(NO3)2 in drinking water for 2, 3, 4, 5, 7, 9 and 11 weeks. The increasing dose and time interval lead to formation of numerous concentric lamellar systems, accumulation of fatty vacuoles, vacuolization of mitochondria, pronounced surface differentiation, and changed shape of the nucleus of Leydig cells. The ultrastructural picture corresponded with an enhanced metabolic activity in some cells; in other cells dystrophic changes were observed in other. In addition to that, some cells were found that are considered by us to be an intermediary stage between the nondifferentiated mesenchymal cells and the fully functional Leydig cells.

Animals↗
PubMed1995

Tissue and serum swainsonine concentrations in sheep ingesting Astragalus lentiginosus (locoweed).

Locoweed intoxication or locoism results when animals continuously graze certain plants of the general Astragalus or Oxytropis. The locoweed toxin, swainsonine, is water soluble and is rapidly absorbed and eliminated. The purpose of this study was to determine the distribution of swainsonine in tissues of sheep eating locoweed and to determine if the tissue swainsonine concentrations change with continued locoweed ingestion. Fifteen cross-breed whethers were divided into 3 groups of 5 each and fed alfalfa pellets (Group 1) or alfalfa pellets with 10% Astragalus lentiginosus for 13 d (Group 2) or for 21 d (Group 3). After the feeding periods, the animals were slaughtered and tissues were collected, frozen and later analyzed for swainsonine using an in vitro, alpha-mannosidase inhibition assay. Significant alpha-mannosidase inhibitory activity (interpreted as ng/ml of swainsonine) was detected in whole blood, skeletal muscle, brain, kidney, liver, thyroid and urine. The swainsonine concentrations in tissues were significantly correlated with daily swainsonine intake (r = 0.58 to 0.96). With the exception of kidney, longer exposure did not result in significant increases in the swainsonine concentrations in blood, muscle, brain, liver or thyroid. Liver had the highest swainsonine concentrations with 3049 +/- 1952 and 3947 +/- 457 ng/ml (mean +/- SD) in Groups 2 and 3 respectively. Swainsonine concentrations varied widely within the groups suggesting individual animal variability in swainsonine absorption, metabolism and excretion. These findings suggest that swainsonine is present in tissues of animals eating locoweed and that in most tissues the amount was directly correlated to the swainsonine dose ingested, but not to the length of exposure.

Animals↗
PubMed1997

Role of exogenous reduced glutathione on time dependent 203Hg distribution in liver and kidney of a freshwater teleost, Anabas testudineus.

Time-dependent tissue distribution of mercury(Hg) was studied in a freshwater perch, Anabas testudineus which revealed that the liver and kidneys are the major sites of Hg retention. The role of reduced glutathione (GSH) in the clearance of Hg was also investigated to evaluate the ameliorative effect of this nucleophile. For this purpose, the perch was given GSH 15 min before or after they received 203Hg by injection. The fish were then sacrificed at 24 h and 48 h later. The results clearly indicate that exogenous GSH can significantly reduce Hg retention in both the liver and kidneys, demonstrating a direct role of this nucleophile in the amelioration of Hg-induced toxicity in the early phase of intoxication.

Animals↗
PubMed2007

Mouse inbred strain differences in ethanol drinking to intoxication.

Recently, we described a simple procedure, Drinking in the Dark (DID), in which C57BL/6J mice self-administer ethanol to a blood ethanol concentration (BEC) above 1 mg/ml. The test consists of replacing the water with 20% ethanol in the home cage for 4 h early during the dark phase of the light/dark cycle. Three experiments were conducted to explore this high ethanol drinking model further. In experiment 1, a microanalysis of C57BL/6J behavior showed that the pattern of ethanol drinking was different from routine water intake. In experiment 2, drinking impaired performance of C57BL/6J on the accelerating rotarod and balance beam. In experiment 3, 12 inbred strains were screened to estimate genetic influences on DID and correlations with other traits. Large, reliable differences in intake and BEC were detected among the strains, with C57BL/6J showing the highest values. Strain means were positively correlated with intake and BEC in the standard (24 h) and a limited (4 h) two-bottle ethanol vs. water test, but BECs reached higher levels for DID. Strain mean correlations with other traits in the Mouse Phenome Project database supported previously reported genetic relationships of high ethanol drinking with low chronic ethanol withdrawal severity and low ethanol-conditioned taste aversion. We extend these findings by showing that the correlation estimates remain relatively unchanged even after correcting for phylogenetic relatedness among the strains, thus relaxing the assumption that the strain means are statistically independent. We discuss applications of the model for finding genes that predispose pharmacologically significant drinking in mice.

Alcohol Drinking↗
PubMed2003

The hepatoprotective effects of Limonium sinense against carbon tetrachloride and beta-D-galactosamine intoxication in rats.

In the present study, the hepatoprotective action of Limonium sinense (Plumbaginaceae) was evident after carbon tetrachloride (CCl(4)) and beta-D-galactosamine (D-GalN), respectively, challenge in rats. The plant materials were divided into two parts: (1) the roots extracted with water (WRE) and (2) the leaves extracted with methanol and fractionated with chloroform (CLE). Both WRE and CLE were extremely flavonoid-enriched extracts. In an CCl(4)-induced acute liver damage study, pretreatment with WRE at 300 mg/kg i.p. and CLE at 100 mg/kg i.p. significantly reduced the amino-transaminases levels of SGOT (p < 0.01) and SGPT (p < 0.01) previously increased by CCl(4) intoxication. In D-GalN-induced acute liver damage study, administration of WRE (300 and 500 mg/kg) or CLE (100 mg/kg) p.o. also significantly reduced the SGOT (p < 0.01) and SGPT (p < 0.01) levels previously increased by D-GalN intoxication. Furthermore, the serum triglyceride level was increased after pretreatment with WRE or CLE previously reduced by D-GalN intoxication. All of the liver function profiles were confirmed to have improvement of liver lesion in histopathological observation. In an acute toxicity test on ICR mice, the LD(50) of WRE was 777.6 mg/kg i.p. An in vitro study showed that CLE possessed a more potent cytotoxicity to human hepatocellular carcinoma cells (Hep3B) (EC(50) = 43.1 micro g/mL) than the other organic fractions, which were fractionated from methanol extracts of the leaves of L. sinense. The present results conclude that L. sinense possesses a hepatoprotective efficacy, and is relatively safe in rats.

Administration, Oral↗
PubMed2003

Activity of pancreatic antioxidative enzymes and malondialdehyde concentrations in rats with hyperglycemia caused by fluoride intoxication.

The aim of this work was to examine the effect of fluoride ions on antioxidative enzyme activity in the pancreas of rats exposed during 4 months to NaF in drinking water. The study was carried out in 30 four-week-old male Wistar FL rats, that were randomly assigned to three equal groups and given distilled water ad libitum for three weeks. Subsequently, two examined groups of animals were exposed to NaF in drinking water: group 1 (10 rats) at 50 mg F(-)/L (2.63 mmol/L), group 2 (10 rats) at 100 mg F(-)/L (5.26 mmol/L). The control group (10 rats) received distilled water. After 4 months the animals were anesthetized with ether prior to collection of pancreas and cardiac blood. Serum concentrations of glucose and fluoride, as well as activities of the cytoplasmic (CuZn-SOD) and the mitochondrial (Mn-SOD) superoxide dismutase, glutathione peroxidase (GSH-Px) and concentrations of malondialdehyde (MDA) in the homogenized pancreas were measured. The activity of CuZn-SOD was reduced by 50% and a tendency to lower activities of Mn-SOD was observed. No changes were noted in the activity of GSH-Px or concentrations of MDA. We conclude that: 1) the fluoride caused hyperglycemia in rats in this study is not accompanied by an activation of the free radical production in the pancreas; 2) the hyperglycemia in the exposed rats cannot be attributed to pancreatic damage caused by fluoride ions (the cause in this case appears to be extrapancreatic); 3) the inhibition of pancreatic CuZn-SOD is probably due to the direct action of fluoride on the enzyme.

Animals↗
PubMed1980

[Intoxication and detoxication of heavy metals by humic acids].

Humic acids are naturally occurring phenol body polymerisates which form chelate compounds with heavy metals. Their wide occurrence in soils and surface waters has made them a major reactant to toxic and essential heavy metals in the biosphere. Humic acids, by ways of fixation or solution of trace elements or change of their own toxicological parameters, may exercise influence on ecological circulation, depending on both pH and ion strength of the medium concerned. While the detoxicating action of humic acids is likely to play the major role in natural ecosystems, their effects on heavy metal ion toxicity to experimental animals were found to depend on the technique of application. Enzymatically synthesized phenol body polymerisates are considered to be appropriate model substances for further studies into correlations between humic acids, on the one hand, and heavy metals, on the other.

Animals↗
PubMed1980

Reversible microcytic hypochromic anaemia in dialysis patients due to aluminium intoxication.

Twelve patients being treated by intermittent haemodialysis developed a severe microcytic hypochromic anaemia despite adequate iron supplements. Serum ferritin concentration was normal or high. Seven patients later developed histologically proven fracturing osteomalacia and one a fatal encephalopathy. Plasma aluminium concentration was high in all twelve patients and the source was the water used to make up dialysis fluid. Following dialysis with aluminium free dialysis fluid, plasma concentrations of aluminium fell, red cell morphology returned to normal and haemoglobin rose. We believe that in addition to causing encephalopathy and osteomalacia, aluminium causes a microcytic hypochromic anaemia. This anaemia appears to be the first manifestation of aluminium intoxication and is reversed by removing the source of aluminium.

Adult↗
PubMed2003

Food and water consumption in assessment of acute oral toxicity of HEPALIP FORTE in rats.

Body weight variations during toxicological testing can be one of the indicators of the test substance toxic effects. Data on food and water consumption are true indicators of the rate of growth of experimental animals (Stevens & Gallo, 1989). Daily recording of the food and water consumption was done during the acute toxicity testing of HEPALIP FORTE. The study was performed on Wistar rats. The active component of HEPALIP FORTE is EPL substance--essential phospholipids, a natural substance present in every living cell. Essential phospholipids in combination with vitamins have been used in the treatment of liver diseases, dyslipoproteinaemias and intoxications accompanied with liver failure. Statistical analysis of the body weight variations was performed separately, for males and females. The analysis failed to show any significant difference between the groups. There was a significant difference in water consumption between the male group 2M and female groups 3F and 2F in comparison with control groups. Statistical analysis of the variations of food consumption showed a significant difference in all male groups in comparison with control groups, and only in the 3F female group in comparison with a control group. Considering the absence of lethality and the lack of significant influence of the test substance on animal body weights, we concluded that the test substance was not acutely toxic in rats, if applied orally, in single doses of 300 mg/kg, 500 mg/kg and 1000 mg/kg. Significant differences found in food and water consumption suggest a need of their during the future chronic toxicity testing.

Journal Article↗
PubMed2002

Neuropathology of skin denervation in acrylamide-induced neuropathy.

Previous studies have established the neurotoxicity and pathology of acrylamide to large-diameter nerves. It remains unclear (1) whether small-diameter sensory nerves are vulnerable to acrylamide and (2) if so, how the pathology evolves during intoxication. We investigated the influence of acrylamide on small-diameter sensory nerves by studying the pathology of sensory nerve terminals in the skin. The neurotoxic effects of acrylamide (400 ppm in drinking water) on mice were assessed by immunostaining the skin with protein gene product 9.5, a ubiquitin C-terminal hydrolase, particularly useful for demonstrating cutaneous nerve terminals. Within 5 days of acrylamide administration (the initial stage), epidermal nerves showed two major changes: (1) terminal swelling and (2) increased branching. There was a progressive reduction in epidermal nerve density (END) thereafter. Fifteen days after acrylamide intoxication (the late stage), reduction in END became evident (25.22 +/- 2.19 fibers/mm vs 41.74 +/- 2.60 fibers/mm in control mice, P < 0.003). At this stage, there was significant dermal nerve degeneration with ultrastructural demonstrations of vacuolar changes. These findings establish the pathological consequences of acrylamide neurotoxicity in cutaneous sensory nerves with far-reaching implications: (1) providing an animal system to study "dying-back" pathology of nociceptive nerves and (2) forming the ultrastructural foundation for interpreting the pathology of cutaneous nerve degeneration in skin biopsies.

Acrylamide↗
PubMed1996

Spatial learning in rats exposed to acute ethanol intoxication on gestational day 8.

Pregnant Wistar rats were treated on gestational day 8 (GD 8) with two IP injections of either ethanol (2.9 g/kg in 24% v/v saline solution) or saline. Offspring were tested in the water-maze task at 45 or 90 days of age. The escape latencies of rats trained with a submerged escape platform at a fixed location were similar between control and experimental rats. Analyses of responses on a probe trial carried out 10 days after the training period, revealed that 90-day-old females prenatally exposed to alcohol were less likely to swim in the target region. No differences were observed in this free-swim trial in 45- and 90-day-old male, and 45-day-old female animals. Binding studies of low-affinity GABAA sites in the hippocampus showed an increase in affinity of [3H]GABAA for their binding sites in 90-day-old female offspring prenatally intoxicated with ethanol. Our results demonstrate that acute intoxication with ethanol on GD 8 did not modify acquisition but impaired the retention of spatial learning only in adult female rats. It is possible that the impaired retention will be consequence of higher GABAA receptor affinity.

Alcoholic Intoxication↗
PubMed1986

Stimulation of astrocytes affects cytotoxic brain edema.

Cytotoxic brain edema has been produced in rats by subacute intoxication with triethyltin (TET). Some animals were allowed to recover spontaneously, others were post-treated with an extract of Ginkgo biloba (EGB) for 1 to 4 weeks, beginning 3 days after intoxication was stopped. The time course of the resolution of the edema was studied biochemically and morphologically by light microscopy, histochemistry and electron microscopy (EM). Morphometric evaluation showed that the spontaneous reabsorption of TET-induced edema was very slow: it was evident only 2 weeks after ending TET administration and it required more than 4 weeks to be completed. EGB therapy markedly decreased the vacuolation, as well as the abnormal levels of water and sodium contents, 1 week after beginning the treatment. Less influence of EGB was observed at the later stages. During spontaneous recovery, astroglial cells in the edematous white matter of TET-intoxicated animals showed short and swollen processes containing few organelles, low levels of NADH- and NADPH-tetrazolium reductase activities and glial fibrillary acidic protein (GFAP)-immunofluorescence for about 2 weeks. During EGB therapy the astrocytes regained their cellular processes, containing intense oxidative enzyme activities and GFAP-immunofluorescence as early as after 1 week of treatment. In the EM, astrocytes often appeared hypertrophic, surrounding myelin vacuoles and displaying phagocytosis of myelin debris. We conclude that EGB can accelerate the reabsorption of TET-induced cerebral edema and improve the astroglial reaction.

Animals↗
PubMed2002

Orally delivered alprazolam, diazepam, and triazolam as reinforcers in rhesus monkeys.

RATIONALE: Benzodiazepines are among the most frequently prescribed drugs and are usually taken by mouth. However, there have been few studies of oral self-administration of these drugs, and the results of IV self-administration studies indicate that benzodiazepines are modest reinforcers. OBJECTIVES: To determine if orally delivered alprazolam, diazepam, and triazolam could serve as reinforcers for rhesus monkeys, and to determine some of the conditions under which benzodiazepine reinforced behavior occurs. METHODS: Diazepam or midazolam was initially established as a reinforcer by a fading procedure whereby increasing concentrations were added to a 1 or 2% ethanol solution, and subsequently the ethanol concentration was decreased in steps to zero. Diazepam- and midazolam-reinforced responding persisted in the absence of ethanol. Triazolam and alprazolam served as reinforcers when substituted for diazepam or midazolam. RESULTS: Alprazolam, diazepam, and triazolam served as effective reinforcers across a wide range of concentrations and under fixed-ratio sizes of 16 and 32. Rates of responding were usually far higher than that for the concurrently available vehicle, water. Drug intake (mg drug/kg body weight) generally increased with increases in drug concentration. When large drug amounts were consumed, signs of intoxication were observed. CONCLUSIONS: In contrast to reports of low response rates and weakly maintained behavior, the present results show that the three benzodiazepines can serve as effective reinforcers.

Administration, Oral↗
PubMedDate not supplied

[Neurologic symptoms in lithium poisoning].

A 69-year-old female patient is reported who had been treated with lithium salts for bipolar affective disease. During hospital stay due to myocardial infarction in cardiology department signs of intoxication with lithium carbonate developed. Parkinsonian syndrome and amnesia with abnormal EEG tracings were observed. After withdrawal of lithium and correction of water and electrolyte disturbances as well as pharmacological treatment gradual disappearance of neurological abnormalities was observed, with full normalization of EEG tracings.

Aged↗
PubMed1983

[Changes in MAO activity in the rat liver after chronic exposure to cadmium and lead].

The effect of lead and cadmium on male progeny of the intoxicated Wistar rats was studied. Cadmium (5 ppm), lead (50 ppm), and combined doses of the two were administered in buffered drinking water. The activity of MAO was determined in liver homogenates of young rats at 30, 60 and 90 days of age, using a spectrophotometric method by Mc Even and Cohen with benzylamine as a substrate. In 30-day-old rats the enzyme activity decreased, the values being: Cd - 37,9%, Cd + Pb - 43.1%, Pb - 97.7%, as compared to controls. At 60 days of age the increase observed was: Pb - 100.3%, Cd - Pb - 196%, and Cd - 94.6%, while at 90 days of age the values were: Cd - 80.4%, Cd + Pb - 96.5%, and Pb - 122.7%.

Aging↗
PubMed1994

Chronic lead exposure induces astrogliosis in hippocampus and cerebellum.

The aim of this study was to characterize the cytoskeletal intermediate filaments, glial fibrillary acidic protein (GFAP), and vimentin in normal and lead treated rats, and to compare the astroglial response in the cerebellum and the hippocampus -two regions with great susceptibility to the toxic effects of lead. Experiments combined light and electron microscopy immunohistochemistry using antibodies to GFAP and to vimentin, and conventional transmission electron microscopy techniques. Chronic lead administration was provided through the drinking water (1 g% lead acetate solution) and started when pups were 7 days old through the mother's milk. Following weaning lead intoxicated offspring were continuously exposed during 9 months, and sacrificed, with their corresponding controls, by perfusion-fixation at 30, 60, 75, 90, 180 and 270 days of lead exposure. After 60 and 90 days of treatment, hypertrophic astrocytes were observed in the cerebellum and hippocampus. Additionally, in the same time-period more GFAP immunolabelled astrocytes were detected in the cerebellum but not in the hippocampus. These qualitative observations were confirmed by computerized image analysis quantification. This effect was transient, even though the lead treatment was prolonged for 9 months and the blood-lead levels remained high after 30 days of the lead-exposure. After 90 days of lead administration, hypertrophic astrocytes started to decline and a gradual increment in the number of dense bodies, lipofuscin-like, was evidenced in astrocytes, neurons, pericytes and microglial cells. The data suggest that chronic lead exposure induces an astrocytic reaction as a result of a direct action of lead on astroglial cells or as a response to underlying neural damage.

Animals↗