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At least 1,621 records · Page 90Linked to original sources
PubMed2006

A water extract of Artemisia capillaris prevents 2,2'-azobis(2-amidinopropane) dihydrochloride-induced liver damage in rats.

A water extract of Artemisia capillaris Thunberg (Compositae) was investigated for protective effects against oxidative stress induced by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) in Sprague-Dawley male rats. Rats were orally administered A. capillaris water extract (ACWE; 7.5 g/kg) for 7 days before AAPH treatment (60 mg/kg). AAPH intoxication significantly elevated enzyme markers of liver injury (glutamic oxaloacetic transaminase and glutamic pyruvic transaminase). The pre-administration of ACWE significantly reduced the liver-damaging effects of AAPH as indicated by the low levels of these enzymes. Moreover, the ACWE administration significantly attenuated the accumulation of thiobarbituric acid-reactive substances in both plasma and liver tissues compared with those of rats administered AAPH alone. Furthermore, ACWE administration slightly improved the liver reduced glutathione levels and enhanced the production of antioxidant enzymes like catalase. A. capillaris contained 10.1 mg of catechin in 100 g of dried sample; the high-performance liquid chromatography results showed catechin composition in the ACWE to be 28% (-)-epigallocatechin gallate, 49% (-)- epigallocatechin, and 23% other catechins. These observations clearly indicate that ACWE contains antioxidant catechins capable of ameliorating the AAPH-induced hepatic injury by virtue of its antioxidant activity.

Alanine Transaminase↗
PubMedDate not supplied

Chronic lead intoxication affects the myelin membrane status in the central nervous system of adult rats.

The aim of the experiments presented here was to discern whether prolonged consumption of leaden water, which imitates an environmental exposure, affects the structure of myelin in the central nervous system of adult rats and whether the observed morphological destruction is reflected in biophysical and/or biochemical changes. The results indicated that during chronic lead (Pb) intoxication, the Pb level of the myelin fraction increases significantly. Electron microscopy studies show that myelin in control experiments is built up of ordered layers, whereas in a Pb-intoxicated sample, this order is destroyed in large areas of all preparations. Morphological disturbances in Pb-intoxicated in vivo myelin were reflected by changes in myelin membrane fluidity measured by spectrofluorometry and electron paramagnetic resonance (EPR). Prolonged Pb toxicity also caused significant changes in the morphological structure of oligodendrocytes, an increase of phosphatidylethanolamine, and decrease of protein SH group levels. Simultaneously, we found that the protein and total phospholipid content and levels of phosphatidylinositol, sphingomyelin, phosphatidyloserine, cholesterol, and the pattern of total myelin protein obtained by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) in Pb-intoxicated myelin did not change compared to control values. Also, Pb intoxication did not induce peroxidation by itself and did not accelerate peroxidation produced by iron (Fe) in brain myelin.

Animals↗
PubMed1998

Systemic administration of atipamezole, a selective antagonist of alpha-2 adrenoceptors, facilitates behavioural activity but does not influence short-term or long-term memory in trimethyltin-intoxicated and control rats.

The present study used trimethyltin (TMT)-intoxicated rats as a model for the behavioural syndrome seen after neuronal damage to the limbic system. Behavioural assessments indicated increased locomotor activity and reduced number of groomings in an open-arena task in TMT-intoxicated (6.6 mg/kg as a free base) rats, as has been found previously. A novel finding was the severe deficit in swimming to a visible platform in the water maze task, with reduced swimming speed at the beginning of the training period. During the reacquisition phase of a radial arm maze task, TMT-intoxicated rats made more short-term and long-term memory errors, and their behavioural activity was increased in comparison with controls. The administration of atipamezole (300 micrograms/kg), a selective antagonist of alpha 2-adrenoceptors, enhanced locomotor activity compared to saline-treated rats, but these effects did not differ between the TMT group and their controls. Atipamezole did not enhance short-term or long-term memory in either TMT or control groups. Taken together, the present data indicate that TMT intoxication is a model for global dementia rather than for a specific loss of relational memory. Previous studies on the neurochemical effects of TMT and the alleviation or prevention of neurotoxicity of TMT are reviewed.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed2000

Metabolism of [3alpha-3H] 25-hydroxyvitamin D2 in kidneys isolated from normal and vitamin D2-intoxicated rats.

With the availability of A-ring labelled 25OHD2, [3alpha-3H] 25OHD2, we have performed the present study to examine the metabolism of 25OHD2 using physiological substrate concentrations in perfused kidneys isolated from both normal and vitamin D2-intoxicated rats. Our results indicate that [3alpha-3H] 25OHD2 is metabolized into both 24(S),25,28-trihydroxyvitamin D2 [24(S),25,28(OH)3D2] and 24(R),25,26-trihydroxyvitamin D2 [24(R), 25,26(OH)3D2], and the amounts of these two metabolites produced in the kidney of vitamin D2-intoxicated rat were about 3-5 times higher than those produced in the kidney of normal rat. Similar results were also obtained with rat kidney homogenates incubated with [3alpha-3H] 25OHD2. Furthermore, we noted that the production of both 24(S),25,28(OH)3D2 and 24(R),25,26(OH)3D2 in the kidney homogenates of vitamin D2-intoxicated rats increased with the time of incubation and then subsequently decreased. The decrease in both 24(S),25,28(OH)3D2 and 24(R),25,26(OH)3D2 coincided with an increase in the fraction of total radioactivity distributed in the aqueous phase of the kidney homogenates. This finding suggested the possibility of further metabolism of 24(S),25,28(OH)3D2 and 24(R), 25,26(OH)3D2 into polar water-soluble metabolite(s). We then measured the radioactivity in the aqueous phase of kidney homogenates of both normal and vitamin D2-intoxicated rats incubated with [3alpha-3H] 25OHD2. It was noted that the amount of radioactivity in the aqueous phase of kidney homogenates of vitamin D2-intoxicated rats is higher than that present in the aqueous phase of kidney homogenates of normal rats. Thus, our study provides evidence for the first time for the formation of both 24(S),25,28(OH)3D2 and 24(R),25, 26(OH)3D2 under physiological conditions, and the possibility of their further metabolism into as yet unidentified polar water-soluble metabolite(s). As the formation of all these metabolites is increased in the kidney of vitamin D2-intoxicated rats when compared to normal rats, it appears that the increased rate of metabolism of 25OHD2 during hypervitaminosis D2 plays a significant role in the deactivation of 25OHD2.

25-Hydroxyvitamin D 2↗
PubMedDate not supplied

Selenium and lead: mutual detoxifying effects.

Antagonistic toxic effects of selenium and lead were studied in growing rats. Chronic lead intoxication was produced by cutaneous application of lead naphthenate solution (80-200 mg Pb/kg body weight) for a period of 8 weeks and chronic selenium intoxication was induced by giving 5 ppm, 10 ppm and 15 ppm selenium in drinking water. The growth rate and food consumption of rats receiving selenium in addition to lead approached normal rate while animals treated with only one of them showed hampered growth rate and lower food consumption. The enzymatic activity of delta-aminolevulinic acid dehydrase (ALA-D) in whole blood, liver and kidney and liver P-450 enzyme activity were normal in rats receiving both selenium and lead. The enzymic activities assayed were, however, depressed in the animals receiving either lead or selenium. Assay of lead and selenium in liver, brain, kidney and blood was carried out. Rats receiving both metals and higher concentrations of these metals in the organs studied, as compared to those only receiving one component. The data seem to indicate that the effect of selenium on the toxic effects of lead is similar to its protective role against methylmercury intoxication.

Animals↗
PubMed1994

Successful antidote of multiple lethal infections using sustained delivery of difluoromethylornithine by means of ceramic drug delivery devices.

The objectives of this study were (1) to cure multiple infections of trypanosomiasis in rats by the sustained release of DFMO from biodegradable tricalcium phosphate (TCP) and aluminum-calcium-phosphorous oxide (ALCAP) delivery systems, and (2) to determine if the side effects associated with oral administration of DFMO can be avoided by using TCP and ALCAP capsules. Sixty-eight SD male albino rats (235-270 g) were divided randomly into five groups. Each rat in group I (n = 16) was implanted subcutaneously (s.c.) with four TCP capsules (two large TCP (L-TCP), one PLA-impregnated large TCP (IL-TCP) and one thin TCP capsule (TN-TCP)). Rats in group II (n = 16) were implanted s.c. with four ALCAP ceramics (two large ALCAP (L-ALCAP), one PLA-impregnated large ALCAP (IL-ALCAP) and one thin ALCAP capsule (TN-ALCAP)). Rats in groups III (n = 16), IV (n = 4) and V (n = 16) were left without implants. Rats in group III (n = 16) were given 4% (w/v) DFMO (pH 7) in drinking water at the day of inoculation and continued up to 7 days postinoculation. Rats in group IV (n = 4) served as a nontreated group. Rats in group V (n = 16) served as normal controls. The results showed that all rats implanted with with TCP or ALCAP implants had no intoxications symptoms or side effects such as diarrhea during the treatment period. In contrast, rats given DFMO in drinking water exhibited foul-smelling diarrhea during the treatment period. Microscopic evaluation of blood smears collected from rats receiving DFMO chemotherapy showed an occasional or limited number of stumpy shape (SS) trypanosomes. This study suggests that (1) ceramic drug delivery systems are capable of delivering DFMO in a sustained manner for two months, and were able to cure repeated infections of trypanosomiasis; (2) the use of ceramic implants avoided widely fluctuating, irregular levels of DFMO in the body by keeping sustained levels above minimal effective concentrations; (3) ceramic drug delivery systems provide a pharmacological potentiality for drugs such as DFMO which have been withheld from the market because of severe side effects when administered using conventional methods of drug administration; and (4) DFMO-filled ceramic devices can be implanted subcutaneously in animals that face a threat of lethal protozoal infections in highly infested areas of the world.

Administration, Oral↗
PubMed1996

Low-dose (5 mg/kg) desferrioxamine treatment in acutely aluminium-intoxicated haemodialysis patients using two drug administration schedules.

BACKGROUND: According to the recommendations proposed at The Consensus Conference on Diagnosis and Treatment of Aluminium Overload in End-Stage Renal Failure Patients, Paris, 1992 low-dose desferrioxamine (DFO) treatment was applied for the first time in 41 acutely aluminium-intoxicated patients. METHODS AND RESULTS: DFO-related neurological/ophthalmological side-effects were observed in nine of 11 patients with a post-DFO serum aluminium level > 300 micrograms/litre and in two patients of 30 below this level after a single administration of a 5-mg/kg dose of the chelator in the conventional way (i.e. the last hour of a dialysis session). They were no longer observed after introducing an alternative DFO administration schedule (i.e. administration of the chelator 5 h prior to the start of a haemodialysis session; group I: n = 14). A significant decrease in the serum aluminium levels as well as in the post-DFO serum aluminium increment (delta s A1) was observed during the first 6 months, course of low-dose DFO treatment in group I as well as group II (which consisted of patients receiving DFO in the conventional way; n = 27). Low-dose DFO treatment was accompanied by a significant increase in the mean +/- SD serum iPTH levels (group I: 174 +/- 245 up to 286 +/- 285 ng/litre; group II: 206 +/- 272 up to 409 +/- 424 ng/litre; P < 0.005) and the mean corpuscular volume (group I: 80 +/- 6.4 up to 85 +/- 3.7 fL, P < 0.005; group II: 76 +/- 5.0 up to 87 +/- 4.3 fL, (P < 0.0001). Serum ferritin levels significantly decreased in both groups. No further side-effects were observed during the DFO course. Patients in which DFO treatment could be stopped (i.e. subjects in which both serum aluminium and delta sA1 were below 50 micrograms/litre at two successive occasions) before the end of the 6 months' treatment course had a significantly greater residual diuresis (700 +/- 682 ml/min vs 84 +/- 109 ml/24 h). Also, residual diuresis was found to protect against aluminium intoxication as reflected by the values noted in group I versus those in group II. CONCLUSION: The 5-mg/kg DFO treatment provides a safe and adequate therapy for aluminium overload. In severely aluminium-intoxicated patients presenting post-DFO serum aluminium levels above 300 micrograms/litre DFO should be given once weekly 5 h prior to high-extraction dialysis ensuring (i) maximal chelation of aluminium (ii) limited exposure to circulating aluminium noxamine levels, and (iii) adequate removal of the latter compound. Finally, the necessity for a better communication between the local water distribution companies and the dialysis centres is a major lesson that can be drawn from this dramatic intoxication.

Adult↗
PubMedDate not supplied

Distribution of triazolam and alpha-hydroxytriazolam in a fatal intoxication case.

The case of a 77-year-old woman who was found dead in her bathtub with her head clearly above the water line is presented. The decedent had a medical history of depression, liver disease, spinal stenosis, and diabetes mellitus. An empty medication bottle of triazolam was found in the trashcan. At autopsy, no injury or evidence of drowning was found. Toxicological analysis identified triazolam at a concentration of 0.12 mg/L in the heart blood. Triazolam and alpha-hydroxytriazolam were quantitated in the specimens received. The medical examiner ruled that the cause of death was triazolam intoxication and the manner of death was suicide.

Aged↗
PubMed1985

Lifetime lead intoxication: influence on the amygdaloid kindling model of epileptogenesis.

The nature of amygdaloid kindled seizures was studied in adult rats which were intoxicated with lead starting in neonatal life. Lactating females were exposed to lead via the drinking water (0.25% lead acetate) and the litters were continued on this level of lead after weaning at 27 days of age. When compared to controls, levels of lead in the blood and brain were significantly higher in lead-exposed rats, both at the time of weaning as well as postkindling, beyond 150 days of age. Parameters relating to amygdaloid kindled seizures, including the rate of kindling, seizure latency and seizure threshold were not significantly different in lead-treated rats than in controls. However, duration of behavioral seizures and afterdischarges was significantly longer in rats exposed to lead. Our data suggest that, although lead intoxication starting in neonatal life does not appear to affect the susceptibility to development of amygdaloid kindled seizures, it may enhance seizure severity in this model of epileptogenesis.

Amygdala↗
PubMed2001

Beneficial effects of TCP on soman intoxication in guinea pigs: seizures, brain damage and learning behaviour.

Poisoning with the potent nerve agent soman produces a cascade of central nervous system (CNS) effects characterized by severe convulsions and eventually death. In animals that survive a soman intoxication, lesions in the amygdala, piriform cortex, hippocampus and thalamus can be observed. In order to examine the mechanisms involved in the effects of soman and to evaluate possible curative interventions, a series of behavioural, electrophysiological and neuropathological experiments were carried out in the guinea pig using the NMDA antagonist N-[1-(2-thienyl)cyclohexyl] piperidine (TCP) in conjunction with atropine and pyridostigmine. The NMDA antagonist TCP appeared to be very effective in the treatment of casualties who suffered from soman-induced seizures for 30 min: (i)Seizures were arrested within minutes after the TCP injection, confirmed by quantitative electroencephalogram (EEG), after fast Fourier analysis. Three hours after TCP the quantitative EEGs were completely normal in all frequency bands and remained normal during the entire 3-week intoxication period. The power shift to the lower (delta) frequency bands, indicative for neuropathology and found in control animals intoxicated only by soman, was not observed in the soman-TCP group. (ii)The gross neuropathology found in soman control animals within 48 h after soman was prevented in soman-TCP animals and was still absent in 3-week survivors. Instead, ultrastructural changes were observed, indicative of defense mechanisms of the cell against toxic circumstances. (iii)Twenty-four hours after soman, soman-TCP animals were able to perform in the shuttle box and Morris water maze. The beneficial effects of TCP on the performance in these tests during the 3-week intoxication period were very impressive, notwithstanding (minor) deficits in memory and learning. (iv)The increase in excitability after TCP was confirmed by an increase in the acoustic startle response. Taken together, these results confirmed the involvement of NMDA receptors in the maintenance of soman-induced seizures and the development of brain damage. They underline the current hypothesis that cholinergic mechanisms are responsible for eliciting seizure activity after soman and that, most likely, the subsequent recruitment of other excitatory neurotransmitters and loss of inhibitory control are responsible for the maintenance of seizures and the development of subsequent brain damage.

Animals↗
PubMed1981

Acute and chronic effects of aspirin toxicity and their treatment.

Salicylate poisoning remains a major clinical hazard, usually resulting from accidental ingestions in preschool children, suicidal overdoses in adults and teenagers, and therapeutically acquired intoxication in all ages. Alkalemia or acidemia, alkaluria or aciduria, hypoglycemia or hyperglycemia, and water and electrolyte imbalances may occur; nausea, vomiting, tinnitus, hyperpnea, hyperpyrexia, disorientation, coma, and/or convulsions are common. With chronic, therapeutically induced salicylism, these symptoms may be mistaken for symptoms resulting from the illness for which the salicylates were administered. For acute ingestions, the magnitude of the poisoning is clearly dose related. Blood level determinations are good prognostic indicators for acute ingestions but are of limited value in chronic, therapeutically induced salicylism. Fluid and electrolyte management is the mainstay of therapy. Diuresis, hemodialysis, and hemoperfusion are effective, but the latter two rarely are necessary.

Adolescent↗
PubMed1986

The missing gap. A pitfall in the diagnosis of alcohol intoxication by osmometry.

An osmolal gap (a disparity between measured and calculated serum osmolality) may accompany alcohol intoxication. We encountered a patient with methanol toxicity in whom no such gap was present, despite a markedly elevated serum methanol level. Further investigation revealed that serum osmolality had been measured with a vapor pressure osmometer; this technique may not detect volatile solutes such as alcohols. In vitro testing confirmed the insensitivity of vapor pressure osmometry to toxic ranges of both methanol and ethanol. When alcohol toxicity is suspected, an osmolal gap should be sought only if freezing point osmometry is available.

Alcoholic Intoxication↗
PubMed1988

Histochemical detection of the in vivo produced cellular aldehydes by means of direct Schiff's reaction in CCl4 intoxicated rat liver.

A histochemical technique for detection of the in vivo induced cellular aldehydes based on the direct Schiff's reaction is reported in this paper. CCl4-intoxicated rat liver was used as an experimental model. Fresh and non-pretreated rat liver cryostat sections fixed in 10% formol calcium solution and washed in distilled water were exposed to Schiff's reagent. The sections were then immersed in two baths of sodium bisulphite solution, then in water, dehydrated in ethanol, cleared in xylene and mounted in a synthetic anhydrous mounting medium. As Schiff positive areas presented well circumscribed foci which increased with time following intoxication, semi-quantitative planimetric measurements were feasible. The direct Schiff's reaction detects cellular aldehydes in a sensitive, rapid, histologically and topographically estimable way. The appearance of these aldehydes precedes distinctly morphological alterations detectable by other histochemical or histological techniques. No positive results were obtained in control, non-intoxicated rat livers. Inhibition of this direct Schiff's reaction was obtained in positive control rat liver sections preincubated in solutions of aldehyde blockers. Histochemical detection of aldehydes may give useful information on different aspects of tissue and organ intoxication such as their topography, appearance, evolution, extension, consequences and effects of treatment. The direct Schiff's reaction can be considered as a valuable tool in fundamental and applied research dealing with various toxicological, environmental, pathological, cancer-related and therapeutic problems.

Aldehydes↗
PubMed1982

Conduction velocity in nerve fibres with axonal atrophy due to chronic beta, beta'-iminodiproprionitrile (IDPN).

Serial measurements of maximal motor nerve conduction velocity and muscle action potential amplitude were made on 2 groups of rats for up to 16 months. Group A received 0.05% IDPN in drinking water. Group B received a single injection of 1 g/kg i.p. In the chronically intoxicated animals conduction velocity progressively fell compared with control animals, from a reduction of 7% after 4 months to 22% after 13 months. There was no reduction in muscle action potential amplitude. Marked axonal atrophy was found in distal ventral roots. Many grossly dilated axons were present in proximal ventral roots. In the animals which received a single dose of IDPN no electrophysiological changes were found. A few dilated axons were present in proximal ventral roots, but changes were less severe than in Group A. No distal axonal atrophy was demonstrated.

Animals↗
PubMed1983

The effect of naloxone on intragastric ethanol self-administration.

The acute effect of 1.25 and 2.50 mg/kg naloxone was tested in a group of male Wistar rats readily self-administering 10% w/v ethanol intragastrically following 12 days of forced ethanol intoxication. Compared to saline pretreatment, naloxone did not alter 24 hr intakes of food, water or ethanol. However, both does strongly and significantly inhibited lever pressing for ethanol during 2 hr following pretreatment. The results indicate that naloxones's inhibition of ethanol intake does have a transient postabsorptive component, although this component is unlikely to be specific to ethanol.

Alcohol Drinking↗
PubMed1983

Renal excretion of fluoride during water diuresis and induced urinary pH-changes in man.

Fluoride renal clearance (CF) was studied in young healthy subjects with standard clearance technique following administration of 3 mg F as a 30-min constant infusion. High urinary flow rates were induced and experiments were performed under both urinary alkaline and acidic conditions. The data showed that a high urinary flow resulted in maximum fluoride clearance. High water diuresis may therefore be an important part in the treatment of acute fluoride intoxication.

Adult↗
PubMed2002

Genotoxicity investigation of a cyanobacterial toxin, cylindrospermopsin.

Cylindrospermopsin (CYN), a potent cyanobacterial hepatotoxin produced by Cylindrospermopsis raciborskii and other cyanobacteria, is regularly found in water supplies in many parts of the world, and has been associated with the intoxication of humans and livestock. In this study, Balb/c mice were injected via the intraperitoneal (IP) route with a single dose of 0.2 mg/kg CYN. Animals were sacrificed at 6, 12, 24, 48 and 72 h. DNA was isolated from the mouse livers, and examined for strand breakage by alkaline gel electrophoresis (pH 12). Significant DNA strand breakage was observed in the mouse liver exposed to CYN, suggesting that induction of DNA strand breakage is probably one of the key mechanisms for CYN genotoxicity.

Alkaloids↗
PubMed1972

Alcoholysis of the endogenous phosphate esters in rats treated with large doses of ethanol.

1. Monoethyl phosphate was isolated from the liver of rats treated with large doses of ethanol. The (14)C- and (32)P-labelled products were obtained when [2-(14)C]ethanol and [(32)P]orthophosphate respectively were used as the radioactive precursors. 2. The isolated ethyl phosphate preparations were identified by their chemical properties, chromatographic behaviour and enzymic hydrolysis, which, for the (14)C-labelled substrate, resulted in a partial recovery of the administered [(14)C]ethanol. 3. The possibility of artifact formation of ethyl phosphate was excluded by suitable control experiments. 4. It is concluded that ethyl phosphate formed in vivo may be a product of phosphate-catalysed alcoholysis of various phosphate esters. The physiological significance of the possible substitution of water by ethanol in reactions catalysed by hydrolytic enzymes under conditions of acute body intoxication with the alcohol is emphasized.

Amino Acids↗