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PubMedDate not supplied

Acute arsenic intoxication from environmental arsenic exposure.

Reports of acute arsenic poisoning arising from environmental exposure are rare. Two cases of acute arsenic intoxication resulting from ingestion of contaminated well water are described. These patients experienced a variety of problems: acute gastrointestinal symptoms, central and peripheral neurotoxicity, bone marrow suppression, hepatic toxicity, and mild mucous membrane and cutaneous changes. Although located adjacent to an abandoned mine, the well water had been tested for microorganisms only and was found to be "safe." Regulations for testing of water from private wells for fitness to drink are frequently nonexistent, or only mandate biologic tests for microorganisms. Well water, particularly in areas near mining activity, should be tested for metals.

Acute Disease↗
PubMed1995

Rate of Distribution of Eethanol into the Total Body Water.

Nonequilibrium distribution of ethanol in the total body water (TBW) has implications for understanding gross intoxication seen after rapid consumption of alcohol and for certain new clinical monitoring methods where ethanol is used as a tracer. We studied the rate of distribution of ethanol into the TBW from the concentration--time profiles in whole blood after 0.4 g kg(minus sign1) of ethanol was given by intravenous over 15, 30, 45, and 60 min to six female volunteers. We also gave these females 0.6 g kg(minus sign1) over 30 min, and five young males 0.4 g kg(minus sign1) over 30 min. The results suggest that the blood ethanol concentration after rapid infusion can be described by a two-compartment model with first-order distribution kinetics and zero-order (saturated Michaelis--Menten) elimination. Distribution of ethanol occurred with a half-time of 6.6 plus minus 2.6 min (mean plus minus SD). Alcohol intoxication was more pronounced when ethanol was given rapidly. We conclude that predictable differences in the concentration of ethanol between the blood and the peripheral tissues during rapid supplementation of ethanol causes higher concentrations in blood and a more pronounced intoxication.

Journal Article↗
PubMed1989

[Essential biochemical aspects and toxicology of copper].

Cases of chronic copper intoxication of infants via the ingestion of water, as investigated recently in certain regions of Bavaria and the EMs district, have been prompting a quest for additional risk factors which enhance the effect of copper, even though they do limit its frequency rate. The water from water wells, which had been incriminated, was never of a quality standard that would classify it as "drinking water", i.e. as potable water, so that one must consider not only physiological/biochemical but also water-conditioned/chemical causes. Copper alone as the sole risk factor--and in the concentrations considered to be suspect so far--will not suffice to explain the number of cases recorded to date. Basing on the established knowledge in toxicology and essentially of copper we arrive at the following points of attack for further research on the causes: Special kinds of copper ingestion of a chemical nature; unusual reaction of the intestinal mucosa to copper; development-conditioned variable coeruloplasmin synthesis or elimination of copper via the bile; delayed degradation of metallothioneine. Until the causes have been definitely clarified, we believe that suitable prophylactic measures should be taken in accordance with the short communication by Eife and Müller-Höcker (Dt. Arztebl. 85 (1988) 11: A 693) or the press release by the Federal Public Health Service dated 18 March 1988.

Adult↗
PubMed1989

Endemic fluorosis with spinal cord compression. A case report and review.

We report a case of spinal cord compression in a Mexican immigrant due to vertebral osteosclerosis from chronic fluoride intoxication. Endemic fluorosis is acquired through drinking water. Groundwater sources with high fluoride content occur worldwide. The epidemiology, metabolism, and clinical features of fluorosis are reviewed. Greater physician awareness of this entity is important to identify correctly patients with this unusual and potentially devastating clinical disorder.

Aged↗
PubMed1985

[Risk of bone disease as a result of fluoride intake in chronic renal insufficiency].

Four cases of osteosclerosis were observed in patients with renal failure. All subjects presented with moderate reduction in renal function which had been stabilized for several years. Osteosclerosis appeared progressively but was clinically symptomatic in only one patient. Fluoride intoxication was ascertained on the basis of X-ray examination and bone biopsy. In addition, the source of fluoride intoxication was easily recognized as the drinking water (2 to 3 1/day), "Vichy Saint Yorre" commercial mineral water (fluoride concentration 9 mg/l) in 3 cases, and tap water in the fourth case. These observations emphasize the risk of high chronic fluoride intake in patients with renal failure, even with mild reduction of glomerular filtration rate.

Adult↗
PubMed1984

Practical toxicologic diagnosis.

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.

Animals↗
PubMed1976

Histopathology of experimental ethambutol intoxication.

Ethambutol was administered to albino rats in their drinking water in doses of 105 to 2,500 mg. per kilogram per day for 18 to 102 days. Sixteen per cent developed bilateral lesions consisting of focal axonal swelling without demyelination, in their optic chiasms and the intracranial portions of their optic nerves.

Animals↗
PubMed1999

Intoxicated sexual risk taking: an expectancy or cognitive impairment explanation?

OBJECTIVE: Two experimental studies tested expectancy and impairment explanations for the association between alcohol consumption and unsafe sexual behaviors. METHOD: Young adults, who were administered alcohol (blood alcohol concentration mean = .08 mg%), placebo or water, rated the likelihood that potential consequences would result from risky sexual practices (Study 1, N = 161) and listed potential consequences that could result from having sex without a condom (Study 2, N = 135). RESULTS: Intoxicated participants reported lower perceptions of risk (mean [+/-SD] = 4.5+/-2.1) than those who received placebo (mean = 5.8+/-1.3) or water (mean = 5.5+/-1.7). Intoxicated participants also listed fewer negative consequences (mean = 1.3+/-1.2) than those who received placebo (mean = 1.5+/-1.2) or water (mean = 2.1+/-1.5). In addition, participants who expected alcohol to disinhibit their sexual behavior reported stronger postdrinking perceptions of benefit (mean = 2.6+/-1.8) and indicated that they were more likely to engage in risky sexual practices (mean = 2.4+/-1.7) than those who did not expect sexual disinhibition (mean = 2.0+/-1.7, benefit; mean = 1.8+/-1.1, involvement). CONCLUSIONS: Results support the hypotheses that (1) alcohol-related impairment reduces the drinker's perception of personal risk, and (2) positive outcome expectancies motivate drinkers to engage in risky sexual practices.

Adult↗
PubMed2006

Long-term behavioral consequences of soman poisoning in mice.

We investigated the long-term (up to 90 days) consequences of soman intoxication in mice on weight, motor performances (grip strength, rotarod) and mnemonic cognitive processes (T-maze, Morris water maze test). First, a relative weight loss of 20%, measured 3 days after intoxication, was evidenced as a threshold beyond which neuropathological damage was observed in the hippocampus. Animals were then distributed into either low weight loss (LWL) or high weight loss (HWL) groups according to the relative 20% weight loss threshold. Compared to controls, both groups of poisoned mice quickly exhibited a decrease in their motor performance subsequent to an acute soman toxicity phase. Then, total motor recovery occurred for the LWL group. Comparatively, HWL mice showed only transient recovery prior to a second decrease phase due to soman-induced delayed toxicity. One month after intoxication, mnemonic cognitive performances of the LWL group were similar to controls while the HWL group did not exhibit any learning skill. Three months after poisoning, compared to controls, the LWL group showed similar mnemonic performances in the maze test but a mild deficit in the Morris water maze task. At the same time, learning skills slightly recovered in the HWL group. Mnemonic cognitive data are discussed in relation to the neuropathology, neurogenesis and sprouting occurring in the hippocampus of soman-intoxicated animals.

Animals↗
PubMed1975

Detection of water-to-blood leakages in heat exchangers for cardiopulmonary bypass.

In the construction of heat exchangers, it is of great importance that when they are in use it shall be impossible for water to leak into the blood, as this might lead to hemolysis, intoxications, air emboli, or infection by microorganisms. In an investigation the aim of which was to discover water-to-blood leakages in the heat exchangers that are generally used during cardiopulmonary bypass, tests were carried out on 17 heat exchangers that are used all over the world and are supplied by five different makers. They included both disposable and nondisposable models. In six stainless steel heat exchangers, water leakages to the blood compartment were detected with the aid of helium. Some of these heat exchangers were brand new and had never been used. The size of the leakages was found to be sufficient to enable them to act as channels for the passage of foreign microorganisms.

Blood↗
PubMedDate not supplied

[Group intoxication with 2-ethoxyethanol as an ethanol substitute].

In this paper the authors presented the group 2-ethoxyethanol intoxication of 8 young men aged between 20 to 22. 50-100 ml of pure compound (diluted with water) was administrated as a drink. In this paper symptoms of acute intoxication to this compound were presented. GC-FID and GC-MS were used as diagnostic tools. The obtained results were compared with the data from available literature.

Adult↗
PubMed1983

Aluminium-induced, reversible microcytic anemia in chronic renal failure: clinical and experimental studies.

Ten chronic hemodialysis patients with severe aluminium (Al) intoxication developed a microcytic anemia despite oral iron supplementation. Their microcytosis was reversible after deionization of the dialysis water. Ten age and sex matched hemodialysis patients who were not Al intoxicated but who had a comparable treatment schedule and time on dialysis had no such microcytosis. In order to investigate a possible direct role of Al we intoxicated uremic rats by daily (6/7 days a week) intraperitoneal injections of 30 nmoles/day of aluminium. After 3 months, the Al-intoxicated uremic rats had a significantly lower hematocrit (34.7%), hemoglobin (12.0 g/dl), and MCV (52.5 fl) than the control, vehicle-injected uremic animals (37.4%, 13.1 g/dl and 60.4 fl., respectively). The reticulocyte counts of the intoxicated rats were increased. Serum iron and transferrin iron binding capacity were unchanged. Thus aluminium intoxication of the uremic organism leads to a microcytic anemia possibly by interfering directly with normal hemoglobin synthesis.

Adult↗
PubMed2004

Antihepatotoxic nature of Ulva reticulata (Chlorophyceae) on acetaminophen-induced hepatoxicity in experimental rats.

Ulva reticulata, a marine edible green alga, is a known source of proteins, vitamins, and sulfated polysaccharides. Though there are many reports in the literature regarding the composition and antiviral property of Ulva sp., studies of the antihepatotoxic property of green seaweeds in animal model are scarce. We have studied the antihepatotoxic nature of this marine green edible alga, U. reticulata, in a hot water extract (150 mg/kg of body weight for a period of 15 days) against acetaminophen- induced hepatotoxicity in experimental albino rats. The acetaminophen-induced rats showed significant elevation in levels of the serum marker enzymes aspartate transaminase and alanine transaminase and of lipid peroxides in liver tissue with decreased levels of antioxidant enzymes such as superoxide dismutase and catalase. The levels of reduced glutathione and vitamins (E and C) were also decreased in the liver tissue of acetaminophen-intoxicated rats. The oral pretreatment with a hot water extract of U. reticulata reduced the hepatotoxicity triggered by acetaminophen considerably by improving the antioxidant status in experimental animals with depleted levels of lipid peroxides. These results indicate that the oral pretreatment with a hot water extract of U. reticulata in rats is effective in reducing the hepatic oxidative stress via free radical scavenging properties, suggesting an antihepatotoxic activity.

Acetaminophen↗
PubMed2000

Improvement of phase I drug metabolism with Schisandra chinensis against CCl4 hepatotoxicity in a rat model.

The seed extract of Schisandra chinensis was investigated in the rat for its restorative or therapeutic effect on Phase I hepatic drug metabolism following intoxication by carbon tetrachloride (CCl4). Male Sprague Dawley rats (220-250 g) were divided into two sets, one included rats with or without CCl4 intoxication, the other included CCl4 intoxicated rats with or without treatment of Schisandra extract. With the treatment regimen, rats received four oral doses of Schisandra (160 mg/kg) or the same volume of water at 8, 24, 32 and 48 h after CCl4 intoxication. A single oral dose (80 mg/kg) of antipyrine, a conventional probe for oxidative drug metabolism, was then administered. The levels of liver serum transaminases and cytochrome P450 were measured and the pharmacokinetics of antipyrine were assessed using a non-compartmental approach via WinNonlin. In comparison to the rats without CCl4 intoxication (t1/2: 2.2 +/- 0.9 h; Cl/F: 0.30 +/- 0.01 L/h/Kg; P450: 0.611 +/- 0.190 nmol/mg protein), CCl4 administration significantly decreased elimination (t1/2: 12.0 +/- 3.9 h) and oral clearance (Cl/F: 0.049 +/- 0.018 L/h/kg) of antipyrine, and markedly reduced the content of P450 (0.075 +/- 0.011 nmol/mg protein). Data obtained from intoxicated animals treated by Schisandra extract, compared to those without treatment, showed significant (p < 0.05) improvement in the t1/2 (4.45 +/- 1.7 h) and Cl/F (0.096 +/- 0.018 ml/h) estimates of antipyrine and a 2-3 fold increase in P450 level (0.190 +/- 0.072 nmol/mg protein). Findings in this study suggest that the seed extract of Schisandra appeared to be a promising agent for the improvement of Phase I oxidative metabolism in the liver damaged by CCl4.

Animals↗
PubMed1989

Axonal transport of neurofilament is accelerated in peripheral nerve during 2,5-hexanedione intoxication.

The neurotoxic compound 2,5-hexanedione (2,5-HD) causes an axonopathy characterized by the presence of neurofilament (NF)-containing enlargements in the preterminal segments of central and peripheral axons. The 2,5-HD axonopathy is a good model for human acquired and inherited giant axonal neuropathies. Recently, we reported that following 2,5-HD administration, axonal transport of NF is markedly and selectively accelerated in the primary visual system. We have now studied slow axonal transport in the sciatic system of rats intoxicated with 0.5% 2,5-HD in drinking water. Following radiolabeling, transported proteins were examined after polyacrylamide gel electrophoresis and fluorography. The bulk of radiolabeled NF subunits was located 30-50 mm from the spinal cord in 2,5-HD treated animals and 10-25 mm in controls. The rate of transport of the three NF subunits was 0.7 mm/day in controls and 1.2 mm/day in 2,5-HD treated animals. The rate of transport of tubulin was not significantly changed. Electrophysiological studies of soleus nerve and muscle showed no evidence of denervation after 6 weeks of intoxication. It is concluded that, following 2,5-HD administration, transport of NF is preferentially accelerated in both central and peripheral axons. A pathogenetic mechanism based on the acceleration of NF transport is proposed, which may explain the formation and the distal or proximal location of NF-containing axonal enlargements in giant axonopathies.

Action Potentials↗
PubMed1988

Rat testis during 2,5-hexanedione intoxication and recovery. II. Dynamics of pyrrole reactivity, tubulin content, and microtubule assembly.

Charles River CD rats (200 g) were intoxicated with 1% 2,5-hexanedione (2,5-HD) in the drinking water for 5 weeks followed by a 17-week recovery period. Pyrrole reactivity of testis proteins increased early during intoxication and then returned toward normal during recovery. Testis tubulin content first increased as germ cells were lost and then fell over time while atrophy was maintained. Purified testis tubulin demonstrated a decreased nucleation time for microtubule assembly at 2 weeks, maintained this alteration throughout intoxication, and then returned to normal assembly kinetics during recovery. The assembly abnormality was accompanied by the presence of a unique crosslinked tubulin species. These findings support the hypothesis that alterations in Sertoli cell microtubules result in germ cell loss following 2,5-HD exposure.

Administration, Oral↗
PubMed1980

Acute fluoride poisoning in a New Mexico elementary school.

Thirty-four persons became ill with acute fluoride poisoning shortly after drinking water in an elementary school in Los Lunas, NM. The water supply of the school was supplemented with a concentrated sodium fluoride solution designed to raise fluoride levels in drinking water to 1 to 5 ppm. Two water samples taken after the incident was reported showed elevated fluoride levels of 375 and 93.5 ppm. Malfunction of a relay switch controlling dilution of the fluoride solution produced toxic fluoride levels in the water. The symptoms of all patients were mild and generally of short duration, with two thirds of patients reporting complete resolution within 24 hours. The bitter, salty taste of the water deterred consumption of large amounts and prevented serious intoxication.

Acute Disease↗