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PubMed1989

Increased methylation of chloroform extractable products and CTP: cholinephosphate cytidylyltransferase in brain membrane preparations from triethyltin-intoxicated rats.

Rats were chronically intoxicated with triethyltin in the drinking water (0.002%) for a period of 15 days. Starting with day 5 of the intoxication period a decrease in the body weight was observed and, in parallel, the development of a cerebral oedema could be followed by measuring white matter density. At the same time, an increase of phosphatidylethanolamine-N-methyltransferase and cholinephosphate cytidylyltransferase activities was noted. This increase might be a compensatory mechanism for counteracting the membrane damages induced by triethyltin.

Animals↗
PubMed1999

Daily intake of copper from drinking water among young children in Sweden.

Copper is an essential trace element that may cause intoxication if intake becomes excessive. Young children are at risk of intoxication because of high consumption of drinking water and immature copper metabolism. The aims of this prospective study were to estimate concentrations of copper in drinking water, volumes of drinking water consumed by children, and children's daily intake of copper. Concentrations of copper in unflushed drinking water were analyzed for 1,178 children living in Uppsala and Malmö, Sweden, and concentrations and amounts of copper consumed from drinking water were estimated for 430 of these children, 9-21 months of age. The study children were from Swedish families, were not enrolled in publicly provided day care, and were not breast-fed more than three times a day. In the initial population, the 10th percentile for copper concentration in unflushed drinking water was 0.17 mg/L, the median was 0.72 mg/L, and the 90th percentile was 2.11 mg/L. In the subpopulation of 430 children, the 10th percentile for daily intake of copper from drinking water was 0.03 mg/L, the median was 0.32 mg/L, and the 90th percentile was 1.07 mg/L. The median daily intake of copper from drinking water was higher in Uppsala, at 0.46 mg, than in Malmö, at 0.26 mg. For groups of children whose families took part in a later prospective diary study, the copper concentration in consumed water could, to some extent, be predicted from the concentration of copper in unflushed drinking water. The lowest concentrations of copper in drinking water were found in households with old water-pipe systems and in those living in detached houses. A large proportion of the young children satisfied their daily requirement of copper solely from drinking water. About 10% of the children had a copper intake above the level recommended by the World Health Organization.

Copper↗
PubMed1977

Brain and blood lead in acute intoxication.

Administering lead acetate in drinking water to adult male rats resulted in an elevated lead content in blood and brain during 11 subsequent days. The brain and blood lead contents were proportional to each other although the interdependency changed according to the cumulative dose and equilibration period. The present data indicate that the permeability of the blood-brain barrier towards inorganic lead may be dose-dependent and saturable with high doses of the metal.

Animals↗
PubMed2001

Acute aluminum encephalopathy in a dialysis center caused by a cement mortar water distribution pipe.

BACKGROUND: In Curaçao, distilled seawater from the water plant was used without further purification for hemodialysis for several decades. A new distribution pipe supplying water to a dialysis center on the island was installed in May 1996. To protect it from corrosion, this pipe was lined on the inside with a cement mortar. Because of the aggressiveness of the distilled water, calcium and aluminum (Al) leached from the cement mortar into the water used to prepare dialysate. This caused a possible hard water syndrome and definite acute Al intoxication. METHODS: We reviewed clinical details and outcome at follow-up, and arranged laboratory and toxicological studies of serum and hemodialysis water. RESULTS: Of the 27 patients who had a similar exposure ( approximately 60 hours) to the contaminated dialysate, 10 died from acute Al encephalopathy, whereas 17 patients had no or only minor symptoms and survived. The nonsurvivors were older (64 +/- 3 years vs. 52 +/- 2 years, P < 0.01) and had a lower body weight (57.5 +/- 5.9 kg vs. 86.5 +/- 4.1 kg, P < 0.01) and lower serum albumin concentrations (33 +/- 1 vs. 36 +/- 1 g/L, P < 0.01). Anuria tended to be more common in the nonsurvivors (8 out of 10 vs. 8 out of 17, P> 0.05). Serum Al concentrations, available in seven nonsurvivors, were significantly higher than in the survivors (808 +/- 127 vs. 255 +/- 25 microg/L, P < 0.01). CONCLUSIONS: The water distribution pipe was lined with a cement mortar that was probably inappropriate for transporting drinking water. Water distribution facilities as well as the dialysis community should be aware of the possibility of Al leaching from cemented water distribution pipes. Similar Al loads appear to induce a more severe intoxication in malnourished, older patients with smaller Al distribution volumes and anuria.

Acute Disease↗
PubMed1992

Specific and sensitive quantitation of 2,2'-dichlorodiethyl sulphide (sulphur mustard) in water, plasma and blood: application to toxicokinetic study in the rat after intravenous intoxication.

A sensitive and specific capillary gas chromatographic method has been developed to measure trace amounts of 2,2'-dichlorodiethyl sulphide (sulphur mustard) in environmental or biological samples. Sulphur mustard was isolated from water or plasma by a solid-phase extraction procedure and from blood by liquid-liquid extraction. The accuracy and precision of the methods were demonstrated using replicate analyses of spiked water, plasma or blood: within-run and between-run variabilities were less than 20%. These analytical methods were used to evaluate the rate of sulphur mustard degradation in water or plasma. Good linear calibration curves, with a detection limit of 45 ng/ml, were obtained for quantitation and determination of sulphur mustard in blood following its intravenous administration to rats. Initial toxicokinetic data were obtained.

Animals↗
PubMed2001

Enhanced brain regional lipid peroxidation in developing rats exposed to low level lead acetate.

Neurotoxicity associated with lead exposure may be the result of a series of small perturbations in brain metabolism, and, in particular, of oxidative stress. Some studies have suggested a lead-induced enhancement on lipid peroxidation as a possible mechanism for some toxic effects of lead. However, there are no reports about the association between lipid peroxidation enhancement and brain lead content. In this study, we determined the concentration of lead and the formation of lipid fluorescence products in the blood, as well as in the parietal cortex, striatum, hippocampus, thalamus, and cerebellum of rats exposed prenatally and postnatally to variable concentrations of lead acetate through drinking water. Pregnant Wistar rats were intoxicated throughout gestation with solutions containing either 320 or 160 ppm of lead. The pups were treated after birth in the same way until 45 days of age. Control animals received deionized water for the same period of time. The developing rats were sacrificed at postnatal day 45 and lead level was assessed biochemically in the blood and different brain regions. Results showed that blood lead levels were increased in a dose-dependent manner. In the brain, lead accumulated preferentially in the parietal cortex, striatum, and thalamus as compared to the control group, while lipid fluorescence products were significantly increased in the striatum, thalamus, and hippocampus of the treated animals. These data suggest that in the brain of rats exposed to lead acetate, lead produces a neurotoxic effect with a complex correlation with both lead regional content and lipid peroxidation.

Animals↗
PubMed1992

Chemical burn with cresol intoxication and multiple organ failure.

In general, immediate water irrigation is recommended for all chemical burns. Very few chemicals cannot be safely washed off the skin with water, however cresol is one of the exceptions. A 40 per cent TBSA cresol chemical burn that subsequently developed systemic intoxication and multiple organ failure is reported. The patient survived after intensive general supportive treatment, repeated haemodialysis and wound care.

Burns, Chemical↗
PubMedDate not supplied

[Potable mineral waters as the correctors of the hormonal and motor-evacuatory disorders in chronic alcoholic intoxication].

Long-term history of alcohol drinking is associated with shifts in basal levels of glucagon, gastrin, cortisol and insulin. The longer history of alcohol abuse, the more pronounced the shifts were. Besides hormonal unbalance, the animals had defective gastrointestinal motility and evacuation. Drinking of mineral water can correct the above disturbances only in short-term alcoholic intoxication.

Alcoholism↗
PubMed1986

Effect of an extract of Ginkgo biloba on triethyltin-induced cerebral edema.

The effect of an extract of Ginkgo biloba was studied on cerebral edema in rats intoxicated with triethyltin chloride (TET). Brains of TET-treated rats showed elevated water and sodium levels and a significant increase in the sodium/potassium ratio. Animals treated with TET plus the extract did not show water and electrolyte changes. The course of intoxication and treatment was studied light- and electron-microscopically. A severe edema with extensive vacuolization was seen in the cerebral and cerebellar white matter. Morphometric measurements revealed a significant decrease in these manifestations of the cytotoxic edema when the animals were treated with an extract of Ginkgo biloba. Thus, we conclude that this extract has a protective effect on the development of a cytotoxic edema in the white matter of the brain.

Animals↗
PubMed2006

23-carboxy-24,25,26,27-tetranorvitamin D3 (calcioic acid) and 24-carboxy-25,26,27-trinorvitamin D3 (cholacalcioic acid): end products of 25-hydroxyvitamin D3 metabolism in rat kidney through C-24 oxidation pathway.

During the past two and half decades the elucidation of the metabolic pathways of 25OHD(3) and its active metabolite 1alpha,25(OH)(2)D(3) progressed in parallel. In spite of many advances in this area of vitamin D research, the unequivocal identification of the end products of 25OHD(3) metabolism through C-24 oxidation pathway has not been achieved. It is now well established that both 25OHD(3) and 1alpha,25(OH)(2)D(3) are metabolized through the same C-24 oxidation pathway initiated by the enzyme 24-hydroxylase (CYP24A1). Based on the information that the end product of 1alpha,25(OH)(2)D(3) metabolism through C-24 oxidation pathway is 1alpha-OH-23- COOH-24,25,26,27-tetranor D(3) or calcitroic acid; the metabolism of 25OHD(3) into 23-COOH-24,25,26,27-tetranor D(3) has been assumed. Furthermore, a previous study indicated 24-COOH-25,26,27-trinor D(3) as a water soluble metabolite of 24R,25(OH)(2)D(3) produced in rat kidney homogenates. Therefore, 24-COOH-25,26,27-trinor D(3) was also assumed as another end product of 25OHD(3) metabolism through C-24 oxidation pathway. We embarked on our present study to provide unequivocal proof for these assumptions. We first studied the metabolism of 25OHD(3) at low substrate concentration (3x10(-10)M) using [1,2-(3)H]25OHD(3) as the substrate in the perfused rat kidneys isolated from both normal and vitamin D(3) intoxicated rats. A highly polar water soluble metabolite, labeled as metabolite X was isolated from the kidney perfusate. The amount of metabolite X produced in the kidney of a vitamin D intoxicated rat was about seven times higher than that produced in the kidney of a normal rat. We then produced metabolite X in a quantity sufficient for its structure identification by perfusing kidneys isolated from vitamin D intoxicated rats with high substrate concentration of 25OHD(3) (5x10(-6)M). Using the techniques of electron impact and thermospray mass spectrometry, we established that the metabolite X contained both 23-COOH-24,25,26,27-tetranor D(3) and 24-COOH-25,26,27-trinor D(3) in a ratio of 4:1. The same metabolite X containing both acids in the same ratio of 4:1 was also produced when 24R,25(OH)(2)D(3) was used as the starting substrate. Previously, the trivial name of cholacalcioic acid was assigned to 24-COOH-25,26,27-trinorvitamin D(3). Using the same guidelines, we now assign the trivial name of calcioic acid to 23-COOH-24,25,26,27-tetranor D(3). In summary, for the first time our study provides unequivocal evidence to indicate that both calcioic and cholacalcioic acids as the end products of 25OHD(3) metabolism in rat kidney through C-24 oxidation pathway.

Animals↗
PubMed1979

Renal function and plasma aldosterone during acute lithium intoxication.

Studies on plasma aldosterone, total serum protein, electrolytes, osmolal concentrations in serum and urine, creatinine, lithium and osmolal clearances were carried out on 14 patients suffering from lithium intoxication. The determinations were done on samples obtained on admission and during the following twelve days of treatment with hemodialysis, sodium chloride loading, or forced diuresis. Plasma aldosterone and total serum protein were increased; serum sodium concentrations and creatinine clearances were decreased on admission. Serum osmolality was normal; urine osmolal concentration was just above that in plasma. The results showed that the lithium intoxicated patients were moderately depleted of sodium and water on admission. Plasma aldosterone, total serum protein and serum sodium were normalized during treatment. Creatinine clearance increased but did not normalize in all patients. Renal concentrating tests were performed in five patients three to four weeks after lithium intoxication. The renal concentrating ability was reduced in all. The elevated plasma aldosterone seen in lithium intoxication might have been a result of sodium and water depletion. It is suggested that impaired renal concentrating ability induced by lithium may make some patients more susceptible to conditions which can lead to sodium and water loss, and thereby to lithium intoxication.

Acute Disease↗
PubMed1982

Microgravimetric analysis of nerve edema.

A technique for microgravimetric analysis of nerve edema was used to demonstrate increased water content in hexachlorophene neuropathy. The method was modified from one used previously to quantify brain edema by using density gradient columns prepared with two nonaqueous fluids of high and low specific gravity. This method revealed a wide separation between hexachlorophene-treated and control nerves. Gradient position was then related to specific gravity, which averaged 1.03426 in hexachlorophene-treated nerves versus 1.04921 for control nerves. This, in turn, was correlated with the percentage of water in the tissue. Water content of hexachlorophene-intoxicated nerves was approximately 10% greater than control nerves. A major advantage of this technique is its sensitivity in detecting edema in small tissue samples.

Animals↗
PubMedDate not supplied

[The role of the vascular factor in the reorganization of water metabolism in denervated liver after bacterial endotoxin poisoning].

Intoxication with bacterial lipopolysaccharide (endotoxin) is accompanied by considerable rearrangements in the systems of blood microcirculation and water metabolism of the liver. These rearrangements are manifested as increased sinusoid area, changed total area of the cytoplasm and nuclei as well as the nucleocytoplasmic ratio in hepatocytes, increased content of total water in the organ, and changed magnetic relaxation properties (spin-lattice and spin-spin relaxation times). Preliminary parasympathetic denervation of the liver (vagotomy) changes the pattern of the organ response to bacterial endotoxin poisoning as indicated by the kinetics of studied morphological and biophysical parameters.

Animals↗
PubMed2005

Effect of oral chronic intoxication with sodium arsenite on murine giardiasis.

Chronic exposure to toxicants alters immune function that can affect the ability of the host to mount a response to infection. Giardiasis is a gastrointestinal disease in which subtle alteration in immunity of the host can transform the normal acute infection into a chronic one. In this work we used a murine giardiasis model to evaluate the effect of chronic oral intoxication with sodium arsenite on the characteristics of giardiasis. BALB/c mice were intoxicated during 45 days with water containing 50, 125 or 250 microg/mL sodium arsenite. Each group was then inoculated with G. muris cysts. Cysts excreted in the feces were isolated and quantified. The toxic effect of arsenic on intestinal trophozoites was evaluated using G. lamblia trophozoites cultured in vitro with different arsenic concentrations, corresponding to equivalent concentrations of arsenic found in the gut lumen of intoxicated mice. Mice intoxicated with 125 and 250 microg/mL of sodium arsenite and infected with G. muris cysts displayed a shorter period of cysts excretion and were resistant to secondary infection with the parasite. In vitro studies showed that G. lamblia trophozoites were able to grow in presence of high sodium arsenite concentrations, suggesting the absence of a direct toxic effect on the parasite in the gut. Since a longer period of Giardia cysts excretion is associated with suppression of the immune system, the earlier clearance of primary G. muris infection in intoxicated mice suggests the induction of an immune modification that leads to an improved ability of mice to overcome the infection.

Animals↗
PubMed2006

Infantile sensitivity to ethanol's motivational effects: Ethanol reinforcement during the third postnatal week.

BACKGROUND: Although tests specific to newborn rats have frequently verified their susceptibility to the reinforcing properties of ethanol, demonstration of comparable reinforcing effects in older infants has been elusive. Using a second-order conditioning procedure, the present study assessed in preweanling rats whether pairing with early postabsorptive effects of ethanol would render intraorally delivered gustatory stimuli capable of positive reinforcement for association with a salient texture. Direct reinforcing effects of ethanol were also evaluated through intake tests of gustatory stimuli previously paired with the drug. Blood ethanol levels (BELs) were determined for each of the ethanol doses used. METHODS: Pups (14 days old) were stimulated with intraoral infusion of sucrose (10% v/v), water, or quinine (0.0045% w/v) 5 minutes after being intragastrically (i.g.) administered 0.00, 0.25, 0.50, or 2.00 g/kg ethanol (Experiments 1 and 2). These stimuli were then briefly presented while pups experienced a rough texture (sandpaper). Rats were subsequently evaluated in a 2-way texture location test (sandpaper vs smooth surface). In Experiment 3, sucrose, water, or quinine was paired with early postabsorptive effects of ethanol (0.00, 0.50, or 2.0 g/kg). Consumption of these stimuli was later assessed. Motor activity patterns during the intake test were also evaluated. In Experiment 4, BELs corresponding to 0.25, 0.50, or 2.0 g/kg ethanol were determined 5 and 20 minutes after i.g. administration (time periods were in accord with the onset and offset of intraoral stimulation used in the previous experiments). RESULTS: Intraoral infusion of sucrose, water, or quinine, while under a state of sobriety and paired with sandpaper, resulted in roughly 50% preference for this texture. Sandpaper preferences were significantly elevated in pups that had experienced sucrose or water in a nonsober state-while under the effects of ethanol (Experiments 1 and 2). This indicated reinforcing effects of the ethanol intoxication. Pairing ethanol intoxication directly with consumption of sucrose, water, or quinine did not affect their later consumption. Yet, there were clear indications that this pairing resulted in conditioned behavioral activity patterns. Blood ethanol levels corresponding to the ethanol doses used here ranged between 10 and 150 mg%. CONCLUSIONS: Infants appear sensitive to pharmacological reinforcing properties of low and relatively high ethanol doses. This sensitivity was revealed indirectly, by pairing gustatory stimuli with ethanol intoxication and then allowing these stimuli to act as second-order reinforcement for a quite different (tactile) stimulus. Behavioral activation elicited by the gustatory stimuli previously paired with a state of intoxication seems to compete with the expression of ethanol's motivational properties as assessed through intake tests.

Animals↗