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PubMed1990

Na+/K(+)-adenosine triphosphatase activity of pulmonary arteries after intoxication with the pyrrolizidine alkaloid, monocrotaline.

Na+/K(+)-Adenosine triphosphatase-dependent activities of K(+)- return relaxation and 86Rb uptake were studied in pulmonary arteries taken from rats with pulmonary hypertension induced by monocrotaline. Rats were given monocrotaline in drinking water, 20 mg/l, for 4 or more days. Isolated arteries were placed in tissue baths and contracted with norepinephrine or 5-hydroxy-tryptamine under K(+)-free conditions. The arteries relaxed when K+ was "returned" to the bath. Compared to arteries from untreated rats, arteries taken from rats pretreated with monocrotaline developed less force in response to contracting agents and did not relax to the same extent. After 4 days treatment with monocrotaline, the rate of relaxation of the arteries in response to K(+)-return was slower than that of arteries taken from untreated rats. Endothelial trauma or in vitro treatment with ouabain produced a similar decrease in the rate of relaxation. Uptake of radiolabeled Rb by perfused arteries was not altered by 4 days of monocrotaline pretreatment. Isolated lungs taken from monocrotaline-pretreated rats (5 days of ingestion of 20 mg/l of monocrotaline drinking water) accumulated similar quantities of 86Rb+ during 40-sec perfusions. Shorter perfusion times, 10 and 20 sec, resulted in greater rates of uptake of 86Rb- by lungs taken from monocrotaline-treated rats. Monocrotaline produced changes in both the mechanical and biochemical properties of pulmonary arteries after only 4 to 5 days. These changes were associated with ouabain-sensitive processes. It appears, therefore, that one of the early targets in monocrotaline intoxication is the Na+/K+ pump of the pulmonary arteries.

Animals↗
PubMed1993

Zinc and copper in the tissues and serum of cadmium intoxicated guinea-pigs: influence of vitamin C.

Cadmium in the dose of 1 mg/animal/day was administered to guinea-pigs in the form of CdCl2 dissolved in drinking water during short-term (5 weeks) and subchronic (12 weeks) experiments. Both the control and cadmium-treated groups were divided into two subgroups, according to low (2 mg/animal/day) and high (100 mg/animal/day) vitamin C intake. Subchronic cadmium treatment caused copper deficiency indicated by a dramatic decrease of copper concentration in the liver and serum and by its moderate decrease in the testes and brain. Cadmium significantly increased zinc concentrations in the kidneys during the whole experiment and decreased the level of zinc in the serum after subchronic cadmium treatment. In the control groups, the levels of zinc and copper in the serum were lowered after 5 weeks of high vitamin C doses. High doses of vitamin C in cadmium-treated guinea-pigs decreased the levels of copper in the testes, brain and serum. These observations suggest that cadmium intake in relatively high doses might potentiate the development of copper deficiency, and high doses of vitamin C aggravate, to a certain extent, copper depletion in some important organs and serum of guinea-pigs.

Administration, Oral↗
PubMed1997

Chronic aluminum intoxication in rats: dose-dependent morphological changes.

The objective of the study was to evaluate the chronic cytotoxic effect of very low nontoxic aluminum (Al) in the drinking water of rats. The control group (10 rats) received deionized water, whereas the two experimental groups (10 rats each) received Al in a dose of 5 mg and 20 mg/kg bw/day, respectively. Al was applied in their drinking water during the 6-month duration of the study. Light and electron microscopy (EM) was performed on several body tissues (i.e., kidney, liver muscle, brain). The results showed distinct dose-dependent changes in kidney and brain. In tubulo-interstitial part of the kidney many proximal tubules were hyperdilated. Their cells were swollen and the microvilli were largely lost. Atrophy of some tubules, surrounded by focal areas of interstitial fibrosis was also observed. Some of the glomeruli were undergoing partial sclerosis and in many focal mesangial hypercellularity was found. No distinct morphological changes in other peripheral tissues were observed. In brain, most pronounced changes were observed in hippocampus: they include spongioform changes in pyramidal layer, nuclear deformity and presence of vaculoes in the nuclei. Neurofibrillary degeneration, similar to neurofibrillary tangles in Alzheimer's disease, was also observed. It can thus be concluded that despite very low gastrointestinal absorption (less than 1%), Al in drinking water might accumulate in the long term in vital organs such as kidney and brain, with distinct cytotoxic and neurotoxic effects.

Aluminum↗
PubMed1995

Effect of acute ethanol ingestion on orthostatic vital signs.

STUDY OBJECTIVE: To determine the effect of acute ethanol intoxication on the results of orthostatic tilt testing. DESIGN: Prospective, randomized crossover study. Subjects received ethanol (1.1 gm/kg) or an equal volume of water added to nonalcoholic beer. Orthostatic vital signs, ethanol concentration, and relative volume status were checked initially and hourly for 8 hours. PARTICIPANTS: Twenty healthy human volunteers, 10 men, and 10 women. RESULTS: Peak ethanol concentration was 116 +/- 18 mg/dL (mean +/- SD) 1 hour after ingestion. ANOVA for repeated measures revealed a significant difference in orthostatic pulse change and relative volume deficit between the ethanol and placebo groups (P < .05). Post hoc testing revealed significant differences between the two groups at two, five, seven and eight hours post ingestion for pulse change, and two to eight hours for volume status (Bonferroni's corrected t test, P < .0055). At 2 and 5 to 8 hours, there were significantly more positive tilt tests (+/- 30 beat/minute increase) in the ethanol group than in the placebo group (P < .05). Starting at 2 hours, the ethanol group had a statistically significant relative fluid deficit averaging .5 L by 3 hours. There was no difference in postural blood pressure changes between the two groups. CONCLUSION: In healthy volunteers, ethanol intoxication resulted in exaggerated postural pulse changes and in a greater proportion of positive orthostatic tilt test results than in a placebo group. These changes were accompanied by significant relative fluid deficits.

Adult↗
PubMed1990

Physiological changes in the sciatic nerve endoneurium of lead-intoxicated rats: a model of endoneurial homeostasis.

The effects of inorganic lead (Pb) on peripheral nerves were studied by measuring the permeability coefficient-surface area product to albumin (PSA) of the blood-nerve interface (BNI), water and Pb content of endoneurium, and residual endoneurial plasma volume (Vp) of sciatic nerves of adult rats maintained on a 4% Pb diet for 2-12 weeks. Additionally, body weight, haematocrit, and blood Pb levels were also monitored. Within 1 week, both blood and endoneurial Pb levels had increased significantly above background levels and continued to increase up to the 6th week. Thereafter, over the next 6 weeks, the blood Pb levels were relatively stable, while the endoneurial Pb levels decreased sharply to a quarter of their peak values. The wet/dry weight ratio of the endoneurium, an indicator of nerve oedema, increased by about 30% from the 4th to 12th week, reaching a water content of 75% corresponding to a 24% increase of the total fascicular area. PSA increased only by the 8th week, without an accompanying increase in Vp. This suggests that the increase in PSA reflects an increase in the permeability of the BNI. Furthermore, the moderate 3-fold increase in PSA is more consistent with an adaptive response of the BNI to changes in the endoneurial microenvironment rather than a massive breakdown or disruption of the BNI. This is supported by the inconsistent or mild leakage of horseradish peroxidase from endoneurial capillaries observed in Pb-intoxicated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Acrylamide and polyacrylamide: a review of production, use, environmental fate and neurotoxicity.

Acrylamide is a highly water soluble vinyl monomer formed from the hydration of acrylonitrile. The major commercial use of acrylamide is the formation of polymers. In the environment acrylamide has a high mobility in soil, may travel great distances in ground-water, is biodegradable, and is not absorbed by sediments or affected by water treatment. It is absorbed by all routes of animal exposure. The main metabolite is N-acetyl-S-(3-amino-3-oxypropyl)-cysteine and is excreted predominantly in the urine. Acrylamide produces an ascending central/peripheral axonopathy in man and animals. The major histological findings are swelling of axons and/or decrease in number of large diameter axons. Acrylamide axonopathy is reversible with time, but full recovery depends upon the severity of the intoxication. All reported cases of acrylamide toxicity have been attributed to handling the monomer. Polyacrylamide is non-toxic. Specific clinical features of acrylamide intoxication are more conclusive than electrophysiological, histological or biochemical laboratory tests for diagnosis. Acrylamide can be detected by titration, colorimetry, high performance chromatography, gas chromatography and polarography in air, water, biological fluids, tissues and polyacrylamides. Present research on the effects of acrylamide focuses on developmental and reproductive effects, genotoxicity and carcinogenicity.

Acrylamides↗
PubMed1963

Liver disease and ammonia intoxication.

The relation between ammonia intoxication and liver disease is not clear. Ammonia appears to be relatively non-toxic to normal individuals, whereas some patients with liver disease appear to be exquisitely sensitive to dietary protein, ammonia-releasing substances, and ammonium salts. In an attempt to elucidate this relationship the intravenous LD(50) of ammonium chloride was determined in both normal mice and in those with liver disease produced by a variety of means. Parenchymal damage was created by acute and chronic carbon tetrachloride intoxication, a low-protein, lipotrope-deficient diet, and mouse hepatitis virus. Mice in which the portal vein had been partially ligated and those infected with Schistosoma mansoni developed portal-systemic collateral circulation. Groups of these mice were placed on high-protein diets and ammonia drinking water for periods as long as two months. A combination of both parenchymal damage and collateral circulation was induced in mice either by bile duct ligation or by a combination of schistosomiasis and acute carbon tetrachloride intoxication. When the above groups of mice with liver disease were compared with normal control mice in the same weight range, the LD(50) of ammonium chloride showed no striking change.

Ammonia↗
PubMed1983

Macromolecular changes in brain stem of morphinized rats.

Incorporation of [3H]valine into trichloroacetic acid-(TCA)-precipitable, water-soluble or membrane-bound material of whole brain and brain-stem did not differ significantly in morphine-intoxicated, morphine abstinent and control rats. The animals were intoxicated with morphine (final dose 340 mg/kg b.w.) for 15 days, using an ingestion method with no impairment of the caloric intake compared to controls. Abstinent rats were withdrawn from morphine for 2 days after 13 days of intoxication. Measurements of [3H]valine or [14C]valine incorporated into soluble or membrane-bound brain stem proteins failed to demonstrate any significant changes in specific protein bands from morphinized rats. Separation was achieved by polyacrylamide gel electrophoresis with or without sodium-dodecyl sulphate (SDS) or by isoelectric focusing. After immunoabsorption chromatography to remove those proteins antigenically similar to serum proteins, an increase in the staining intensity and in incorporation of [3H]valine into two protein bands (with isoelectric points (Ip:s) 5.75 and 7.7) was seen in brain stem from long-term morphine-intoxicated rats. The results show that macromolecular interactions are involved in long-term morphine actions.

Animals↗
PubMed2003

Is elevated plasma lactate a useful marker in the evaluation of pure carbon monoxide poisoning?

OBJECTIVE: To examine whether CO poisoning induces a significant increase in plasma lactate concentration. DESIGN AND SETTING: Prospective observational clinical study in the emergency department and intensive care unit in a university-affiliated teaching hospital. PATIENTS: 146 pure CO poisonings resulting from dysfunction of gas cookers or water heaters. MEASUREMENTS AND RESULTS: Patients were classified into four neurological impairment groups: 37% were severely, 8% moderately, and 45% mildly intoxicated, while 1% were asymptomatic. We found only very mild increases in plasma lactate concentration (median 2.30 mmol/l) which, however, was significantly correlated with the severity of neurological impairment and blood CO concentration (1.41 mmol/l, Spearman's test r=0.3). CONCLUSIONS: Plasma lactate is mildly elevated in pure CO-exposed patients. This mild increase and the extensive overlap between the groups of neurological impairment severity do not suggest the usefulness of systematic plasma lactate measurement in pure CO poisoning.

Adult↗
PubMed1990

Suppression of ethanol-induced cardiac hypertrophy by beta-adrenoceptor blockade.

The effects of D,L-propranolol and its resolved epimers on cardiac size in rats given ethanol, or a control diet containing maltose-dextrin, every 8 h by gavage, for 48 h were assessed. Co-treatment with ethanol plus saline for 48 h resulted in increases of approximately 10% in wet and dry heart weights, and in their proportional measures (g/kg body wt). Cardiac protein content was increased similarly. Administration of D,L-propranolol (10, 20 mg/kg), or L-propranolol (5, 10, 20 mg/kg), suppressed the increases in response to ethanol, D-Propranolol (10, 20 mg/kg) was ineffective in attenuating ethanol-induced increases in heart weights and protein content. Values of total cardiac DNA and fractional water content were unaffected by any of the treatments. Adrenaline and noradrenaline levels in urine were elevated during 48 h of intoxication in all rats given ethanol. The results suggest that severe, subacute intoxication with ethanol induces cardiac hypertrophy. Further, the data implies that the hypertrophy is mediated through activation of cardiac beta-adrenoceptors.

Adrenergic beta-Antagonists↗
PubMed2007

Differences in postmortem urea nitrogen, creatinine and uric acid levels between blood and pericardial fluid in acute death.

Previous studies showed significant differences in postmortem urea nitrogen (UN), creatinine (Cr) and uric acid (UA) levels in heart blood depending on the causes of death, including acute death. In addition, the levels in pericardial fluid approximated the clinical serum reference ranges, and their elevations may be assessed based on clinical criteria. The present study investigated difference between blood and pericardial levels of these markers. Medicolegal autopsy cases (n=556, within 48h postmortem) of the following causes of death were examined: injury (n=136), asphyxiation (n=50), drowning (n=39), fire fatalities (n=99), hyperthermia (n=11), hypothermia (n=8), poisoning (n=26), delayed traumatic death (n=44) and natural diseases (n=143). When serum UN, Cr and UA levels were compared with the pericardial levels, there was an equivalency for delayed traumatic death and chronic renal failure, although each level was markedly elevated. Parallel increases in serum and pericardial UA and/or Cr levels were also observed for hypothermia and gastrointestinal bleeding. However, in drowning cases, the left cardiac and pericardial UN levels were lower than the right cardiac and peripheral levels, suggesting the influence of water aspiration. Significant elevations in serum and pericardial Cr and UA levels with a higher serum/pericardial UA ratio for fatal methamphetamine intoxication suggest progressive skeletal muscle damage due to advanced hypoxia/acidosis. Similar findings were often observed for other acute and subacute deaths. These findings suggest that a comparison between blood and pericardial nitrogenous compounds would be useful for investigating the cause and process of death.

Adolescent↗
PubMed2001

Evidence for PSP in mussels in Trinidad.

Herein we present the first evidence for the presence of Paralytic Shellfish Poison (PSP) in Trinidadian waters. The toxin was found in a meat extract of the mussel, Perna viridis. PSP has not previously been demonstrated in the shellfish of Caribbean islands. The presence of PSP in Trinidad is therefore significant in that it presents an opportunity to better understand the dynamics of PSP and algal blooms in both a region and island environment not normally associated with PSP.P. viridis is not native to Trinidad, but rather originates from eastern Asia. It presented itself only recently in Trinidadian waters. Interestingly, shellfish consumption and algal blooms have had a long history of coexistence in Trinidad without any record of human intoxications. In this context, potential Public Health implications of finding PSP in a non-native shellfish species are briefly discussed.

Animals↗
PubMed1993

[Chronic ethylene glycol poisoning].

Over a six-week period a 60-year-old patient had several unexplained intoxication-like episodes. He finally had severe abdominal cramps with changes in the level of consciousness and oligoanuric renal failure (creatinine 4.7 mg/dl). The history, marked metabolic acidosis (pH 7.15, HCO3- 2.2 mmol/l, pCO2 6.6 mmHg) as well as raised anion residue (43 mmol/l) and the presence of oxalates in urine suggested poisoning by ethylene glycol contained in antifreeze liquid. Intensive haemodialysis adequately eliminated ethylene glycol and its toxic metabolites (glycol aldehyde, glycolic acid). Renal function returned within 10 days, although the concentrating power of the kidney remained impaired for several weeks because of interstitial nephritis. The intoxication had been caused by a defective heating-pipe system from which the antifreeze had leaked into the hot-water boiler (the patient had habitually prepared hot drinks by using water from the hot-water tap). Gas chromatography demonstrated an ethylene glycol concentration of 21 g per litre of water.

Chronic Disease↗
PubMedDate not supplied

Evaluation of reagent strips for the rapid diagnosis of nitrite poisoning.

Two commercial urine test strips based on the Griess nitrite-specific diazonium salt reaction, having sulfanilamide and para-arsanilic acid as substrates, respectively, were studied as qualitative tests in the rapid diagnosis of nitrite/nitrate poisoning. Their usefulness was compared to other rapid tests, such as the sulfanilic acid-1 naphthylamin and diphenylamine blue tests. The practical sensitivity limit to nitrites in plasma and in water of both the reagent strips and SA-1NA test was 0.50 micrograms NO2/mL, while the diphenylamine test, which is not nitrite specific, showed a positive reaction to nitrites in plasma and in water above 50 micrograms NO2/mL and 5 micrograms NO2/mL, respectively. The in vitro assays were evaluated in vivo by the sublethal intoxication of a sheep with nitrite, demonstrating that commercial urine test strips may be useful for the rapid diagnosis of nitrite/nitrate poisoning.

Evaluation Studies as Topic↗
PubMed1999

The effects of acute and chronic alcohol ingestion on outcome following multiple episodes of mild traumatic brain injury in rats.

OBJECTIVE: Recent studies suggest that in some circumstances, alcohol intoxication at the time of severe head injury may be neuroprotective. The objective of this study was to determine the effect of acute and chronic alcohol ingestion on outcome in rodents sustaining multiple episodes of mild traumatic brain injury while intoxicated. METHOD: For two weeks before experimentation, adult male Sprague-Dawley rats received intoxicating levels of 95% ethanol (3 g/kg) or normal saline (NS) every other day by orogastric instillation. On the day of experimentation, the animals were randomized to receive alcohol or NS. Two hours later, the animals received either mild (1.2 +/- 0.4 ATA) fluid percussion injury (FPI) or no injury. The injured animals received a total of three episodes of FPI (once every four days). Mean reflex recovery time (RRT) was determined (seconds +/- SEM) immediately after each episode. Mean latency time (seconds +/- SEM) for Morris Water Maze (MWM) performance was assessed at post-trauma days 11-19. RESULTS: The chronic alcohol-exposed (CA) and the non-alcohol-exposed (NA) animals intoxicated when injured had prolonged escape, righting, and corneal RRTs after each FPI compared with the nonintoxicated injured animals and the non-injured shams. However, the CA animals had significantly shorter RRTs when compared with the NA rats. All the injured animals had MWM deficits on testing days 1-6 compared with the noninjured controls. On the last two MWM testing days, the injured NA animals had significantly better MWM performance than the injured CA rats. CONCLUSIONS: The injured intoxicated CA animals had a more rapid recovery of reflexes compared with the injured intoxicated NA animals. Despite initial MWM deficits, the injured NA rodents eventually began to learn the MWM. The injured CA rats never learned the maze. Under the conditions of this study, acute alcohol intoxication at the time of multiple episodes of minor head trauma did not provide neuroprotection for NA or CA rodents.

Acute Disease↗
PubMed1975

Influence of carbon tetrachloride or riboflavin on liver carcinogenesis with a single dose of aflatoxin b1.

Liver carcinogenesis with a single dose of aflatoxin B1 (7 mg/kg body weight) has been investigated in a group of female Wistar strain rats by repeated biopsies and necropsies. Another group received a subsequent intoxication with carbon tetrachloride by inhalation (approximately 200 doses) and another one was overloaded with riboflavin (25 parts/10(6) in drinking water). The frequency of hepatomata was almost equal in the aflatoxin and aflatoxin-carbon tetrachloride group. It was lowere in the riboflavin-aflatoxin group. In these 3 groups cirrhosis was never present in neoplastic livers. Megalocytosis was the first lesion observed. All tumoral livers had previous or concomitant megalocytosis. This modification was about as frequent, intense and widespread in aflatoxin-CCl4 and aflatoxin groups but appeared much earlier, as did the first hepatoma, in the aflatoxin-CCl4 group. It was less frequent, less intense and less widespread in the riboflavin-aflatoxin group than in the aflatoxin group. There was also a lower frequency of hepatomata in the riboflavin-aflatoxin group, but the difference was not significant due to the too small number of animals involved. The facts are not a proof of the existence of an obligatory link between megalocytosis and carcinogenesis since a slight megalocytosis was observed in the riboflavin group not affected by the neoplastic process. However, the simplest explanation of our results would be to consider that the potential tumour cells are located among the megalocytic cells, without admitting that every megalocyte is obligatorily a precancerous cell. CCl4 seems to act in shortening the time of appearance of megalocytosis. The protective effect of riboflavine should be regarded with more caution.

Aflatoxins↗