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PubMed2004

Effect of fluoride intoxication on lipidperoxidation and antioxidant status in experimental rats.

Fluoride is a potent enzyme poison. Thirty ground water samples from Vellore District, Tamil Nadu, India were analysed for fluoride content and it was revealed that the fluoride content of 24 samples were over and above the permissible limits. In the present study, the experimental rats were orally treated with 25 ppm of fluoride/rat/day for 8 and 16 weeks, respectively, and the levels of lipid peroxidation and antioxidant enzymes were studied to evaluate fluoride intoxication. An increase in the level of lipid peroxides along with a concomitant decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced glutathione content were observed in fluoride administered groups of rats. The altered antioxidant status may be attributed to the increased generation of free radicals.

Animals↗
PubMed2003

Perinatal exposure to lead and cadmium affects anxiety-like behaviour.

The present study examines the effects of early simultaneous exposure to low level of lead and cadmium on anxiety-like behaviour in the rat, and on monoamine levels in the hypothalamus and hippocampus at weaning and adult animals. Rats were intoxicated with cadmium acetate (10 mg/l) and lead acetate (300 mg/l) in drinking water from the beginning of pregnancy until weaning. Maternal co-exposure to lead and cadmium produced mainly alterations in dopaminergic and serotoninergic systems of hippocampus in both age studied, while noradrenaline content in hypothalamus and hippocampus remained unchanged at 75 days of age. The intoxicated rats showed an increased on indices of anxiety on the elevated plus-maze. These long-term changes in anxiety-like behaviour can be related to dopaminergic and serotoninergic alterations detected in hippocampus.

Acetates↗
PubMed1976

Renal elimination of lithium in rats with lithium intoxication.

The relation between urine flow (V), lithium clearance (CLi) and sodium clearance (CNa) was studied in rats given food containing lithium in amounts leading to inhibition of distal reabsorption of water and sodium. Maximum inhibition of the reabsorption of water was reached at serum lithium concentrations of about 1 mM. At higher serum lithium levels the rats developed intoxication due to a lowering of CLi and a consequent rise of the serum lithium concentration. The intoxication was characterized by a proportional decrease of V and CLi. The decrease of V and CLi was not related to changes of CNa. The results indicate that lithium is reabsorbed in the proximal tubules in parallel with sodium and that the lowering of CLi is due to increased fractional proximal reabsorption of lithium and sodium compensatory to inhibition of the distal reabsorption of sodium.

Absorption↗
PubMed1991

Immunosuppression due to chronic Lantana camara, L. toxicity in sheep.

Five sheep were intoxicated with powdered L. camara, leaves at the rate of 200 mg/kg body weight daily for 110 days and another group of four sheep were drenched with distilled water daily for equal number of days which acted as control. The cell mediated immunity of intoxicated and control sheep was assessed with the help of 2,4-dinitrofluorobenzene skin sensitivity test and graft-versus-host reaction and the antibody forming potential of both the groups of animals was measured by haemagglutination against chicken red blood cells antigen. In addition, the phagocytic activity of splenic reticulo-endothelial cells was analysed by nitro blue tetrazolium test. The results indicated significant reduction of both cellular and humoral immunity due to L. camara toxicity. The non-specific phagocytic activity of splenic reticulo-endothelial cells also showed significant reduction due to L. camara, L. intoxication. The present communication constitutes the first report of in vivo immunosuppression due to chronic lantana poisoning in sheep.

Animals↗
PubMed2000

[Digitalis intoxication during the neonatal period: role of dehydration].

BACKGROUND: Despite the great progress which has been made in the treatment of acute digitalis intoxication by digoxin-immune Fab, it still remains a severe complication of cardiotonic therapy. CASE REPORT: A neonate with ventricular septal defect and large left-to-right shunt was treated with digitalis and diuretics at the usual starting doses. An intensive phototherapy was also required because of a hyperbilirubinemia due to glucose-6-phosphate dehydrogenase deficiency. Toxic digoxin accumulation (plasma level 14 ng/mL) was diagnosed three days after the initiation of treatment by the presence of sinus bradycardia and bursts of ventricular fibrillation. Intravenous administration of digoxin-specific antibody Fab fragments (Digidot) was effective, with a rapid improvement of the digitalis poisoning. CONCLUSION: Because of the particularities concerning drug distribution, metabolism and elimination of drugs in the neonatal period, the digoxin therapeutic index is narrow. This case report suggests the involvement of phototherapy and diuretics, which might induce a significant decrease in extracellular water and drug distribution volumes, ultimately promoting the occurrence of an intoxication.

Cardiotonic Agents↗
PubMedDate not supplied

Infant rats respond differently to alcohol after nursing from an alcohol-intoxicated dam.

Our previous studies indicate that rat pups are able to detect the low levels of ethanol (175 mg %) found in the milk of a moderately intoxicated dam. The present study tested the effect of infantile interactions (including suckling) with ethanol-treated mothers on later behavioral responsiveness to ethanol's sensory properties. In Experiment 1, pups suckled from dams subjected to a 2.5 g/kg ethanol dose (i.g.) or water-treated females during postnatal days (PDs) 3, 5, 7, 9, 11, and 13. During PD 15, these pups were exposed to procedures to induce a conditioned aversion to the low level of ethanol (175 mg % in water), with lithium chloride as the unconditioned stimulus. Conditioning was more effective for pups with the prior ethanol experience within the nursing context. Greater responsiveness to ethanol in milk also was found for conditioning control pups that had interacted with intoxicated dams than for those that had interacted with water-treated dams. Experiment 2 determined that interaction with an intoxicated dam was sufficient for altered responsiveness to ethanol, in that the additional conditioning procedures of Experiment 1 were not needed for the effect. Generally, a relatively brief history of infantile interaction with ethanol-intoxicated dams increased later responsiveness to ethanol's orosensory properties. The results suggest that moderately intoxicated dams within the nursing context provide information to the progeny that may lead to the establishment of ethanol-related memories.

Alcoholic Intoxication↗
PubMedDate not supplied

Effect of triethyltin chloride on the central aminergic neurotransmitters and their metabolites: relationship with pathophysiology of aging.

Triethyltin (TET) salt intoxication provokes a myelinic vacuolisation associated with a white matter cerebral edema. The central nervous system disturbances accompanying these phenomena (Na-K-ATPase activity, neurological symptoms, water and sodium cerebral content) can be counteracted by drugs used in age-related brain failure; consequently, TET intoxication could be suggested as an experimental model for studying the aging process. The aim of the present study is to follow-up the biogenic amine concentrations in different brain areas of TET treated rats, knowing that modifications of cerebral amines exist throughout the aging process. The following results are obtained: the cerebral water content of the TET treated rats is significantly increased, confirming the existence of a brain edema. Monoamine concentrations are significantly decreased, specifically noradrenaline (in hypothalamus, mesencephalon, cerebellum); serotonin (in striatum, hypothalamus, mesencephalon); dopamine only in hypothalamus; these are accompanied by an increase of the metabolites 5 HIAA (in striatum and mesencephalon) and HVA (striatum). These modifications are compared to those occurring in physiological aging, and hypothetical mechanisms are reviewed. We conclude that TET intoxication must not be considered as a pathophysiological model of brain aging, but may be considered as a useful pharmacological tool for studying experimental drugs liable to counteract brain age-induced disturbances.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Cocaine intoxication: hyperpyrexia, rhabdomyolysis and acute renal failure.

Cocaine has become the recreational drug of abuse of the eighties. The prevalence of cocaine has been manifesting increases in intoxications and poisonings. Acute overdoses have been associated with hyperthermia, agitation, paranoid ideation, status epilepticus, ventricular fibrillation, ventricular tachycardia, myocardial infarction, coma, and death. This is the first reported case of cocaine intoxication resulting in severe hyperthermia, bizarre behavior, rhabdomyolysis, and acute renal failure. Treatment consisted of cooling via iced intravenous fluids, nasogastric lavage with ice water, and benzodiazepine sedation. To our knowledge, there is no case report which supports the allusions that cocaine intoxication may cause rhabdomyolysis and acute renal failure.

Acute Kidney Injury↗
PubMed2003

Reinstatement of ethanol-seeking behavior by drug cues following single versus multiple ethanol intoxication in the rat: effects of naltrexone.

RATIONALE: A positive relationship exists between chronic ethanol intoxication experiences and the severity of neural hyperactivity and withdrawal seizures. An important possibility is that withdrawal reactions also influence the motivation to obtain and consume ethanol. OBJECTIVES: To test this hypothesis, the effects of ethanol-cues on the recovery of extinguished ethanol-seeking and the reversal of this effect by naltrexone, were determined in non-dependent rats and in rats subjected to single versus repeated ethanol intoxications. METHODS: Rats were trained to self-administer and discriminate between 10% ethanol and water. Instrumental responding then was extinguished and the effects of exposure to ethanol and water cues were determined. Subsequently, rats were divided into three groups and exposed to control vapor (CTRL), to 12-day ethanol vapor prior to withdrawal (SW), or to three cycles of 3-day intoxication experiences (MW), respectively. Following intoxication, reacquisition and breaking point for ethanol self-administration and cues-induced reinstatement of drug-seeking were investigated. RESULTS: Ethanol cues significantly reinstated responding in the pre- and post-dependence test, but no significant differences between groups was observed. However, the ability of naltrexone to attenuate the response-reinstatement was significantly reduced in MW rats. Moreover, in the progressive ratio schedule, the breaking points for ethanol were significantly increased in the MW animals. CONCLUSIONS: The results suggest that repeated intoxication did not enhance cue-induced reinstatement of ethanol-seeking. However, naltrexone effects on cues-induced "relapse" appear to be attenuated in MW rats.

Alcoholic Intoxication↗
PubMed2005

Vascular dysfunction in patients with chronic arsenosis can be reversed by reduction of arsenic exposure.

Chronic arsenic exposure causes vascular diseases associated with systematic dysfunction of endogenous nitric oxide. Replacement of heavily arsenic-contaminated drinking water with low-arsenic water is a potential intervention strategy for arsenosis, although the reversibility of arsenic intoxication has not established. In the present study, we examined urinary excretion of cyclic guanosine 3 ,5 -monophosphate (cGMP), a second messenger of the vasoactive effects of nitric oxide, and signs and symptoms for peripheral vascular function in 54 arsenosis patients before and after they were supplied with low-arsenic drinking water in an endemic area of chronic arsenic poisoning in Inner Mongolia, China. The arsenosis patients showed a marked decrease in urinary excretion of cGMP (mean +/- SEM: male, 37.0 +/- 6.1; female, 37.2 +/- 5.4 nmol/mmol creatinine), and a 13-month period of consuming low-arsenic drinking water reversed this trend (male, 68.0 +/- 5.6; female, 70.6 +/- 3.0 nmol/mmol creatinine) and improved peripheral vascular response to cold stress. Our intervention study indicates that peripheral vascular disease in arsenosis patients can be reversed by exposure cessation and has important implications for the public health approach to arsenic exposure.

Adolescent↗
PubMed2002

Green tea as a potent antioxidant in alcohol intoxication.

Ethanol oxidation to acetaldehyde and next to acetate is accompanied by free radical generation. Free radicals can affect cell integrity when antioxidant mechanisms are no longer able to cope with the free radical generation observed in ethanol intoxication. Natural antioxidants are particularly useful in such a situation. The present study was designed to investigate the efficacy of green tea as a source of water-soluble antioxidants (catechins) on the liver and blood serum antioxidative potential of rats chronically (28 days) intoxicated with ethanol. Alcohol caused a decrease in liver superoxide dismutase, glutathione peroxidase and catalase activities and an increase in activity of glutathione reductase. Moreover, a decrease in the level of reduced glutathione, ascorbic acid, vitamins A and E and beta-carotene were observed. The activity of serum glutathione peroxidase decreased while glutathione reductase activity increased. The level of serum non-enzymatic antioxidants was also decreased in the liver. Alcohol administration caused an increase in the liver and serum lipid peroxidation products, measured as thiobarbituric acid-reactive substances. However, green tea prevents the changes observed after ethanol intoxication. Green tea also protects membrane phospholipids from enhanced peroxidation. These results indicate a beneficial effect of green tea in alcohol intoxication.

Alcoholic Intoxication↗
PubMed2004

Green tea protection against age-dependent ethanol-induced oxidative stress.

Ethanol intoxication leads to oxidative stress, which may be additionally enhanced by aging. The aim of this study was to investigate the influence of green tea as a source of water-soluble antioxidants on the ability to prevent oxidative stress in aged rats sub-chronically intoxicated with ethanol. Two-, 12-, and 24-mo-old male Wistar rats were divided into 4 experimental groups: (1) control, (2) green tea, (3) ethanol, and (4) ethanol and green tea. Ethanol intoxication produced age-dependent decrease in the activity of serum superoxide dismutase, glutathione peroxidase, and reductase and in levels of glutathione (GSH), vitamins C, E, and A, and beta-carotene. Changes in the serum antioxidative ability were accompanied by enhanced oxidative modification of lipid (increase in lipid hydroperoxides, malondiadehyde, and 4-hydroxynonenal levels) and protein (rise in carbonyl group levels). Green tea partially protected against changes in antioxidant enzymatic as well as nonenzymatic parameters produced by ethanol and enhanced by aging. Administration of green tea significantly protects cellular components such as lipids and proteins against oxidative modification. Results indicate that green tea effectively protects blood serum against oxidative stress produced by ethanol as well as aging.

Aging↗
PubMed2001

Effect of chronic lead exposure on kidney function in male and female rats: determination of a lead exposure biomarker.

Several cytotoxic chemical pollutants inducing peroxidative damages are liable to induce kidney failure. Among these pollutants we find heavy metals such as: lead, nickel, cadmium, vanadium and mercury. Lead is one of the most dangerous metals because it is widely spread in the environment, and because it may be a source of several nervous diseases. The aim of this study is to provide evidence concerning the effect of this metal on the renal function and to try to determine a storage corner in the organism which serves as an indicator of a lead intoxication. Lead acetate was administered by oral route in the drinking water to adult rats aged three months at the rate of 0.3% (P1) and 0.6% (P2). Reference rats received distilled water to drink under the same conditions. The treatment continued for 15, 30, 45, 60 and 90 days. The creatinemia, uremia, glycemia and creatinuria are determined by colorimetric techniques. Lead concentration in blood as well as the lead content of the tail are determined by atomic absorption after nitroperchloric mineralization at the liquid stage. The results showed an increase of creatinemia on the 30th day of the experiment for both sexes in (P1 and P2). The same happened for ureamia. The increase of these two parameters would indicate a renal deficiency which is confirmed by a decrease of creatinuria and urinary pH observed mainly on and after the 45th day of the experiment. An increase of the renal relative weight was noticed in P1 and P2 on the 30th day of the treatment. The determination of the concentration of lead in the blood shows that this factor increases among treated subjects in a constant way, independently of the dose and the duration of the treatment. Nevertheless, the rate increase of lead in the tail seems to be dose-dependent. In conclusion, lead administered by oral route causes a renal deficiency to the rat without distinction between males and females. In addition, the tail seems to be a reliable exposure biomarker that demonstrates lead intoxication. The tail seems to be a dosimeter of lead bio-accumulation. It constitutes an endogenous source of lead impregnation. The concentration of lead in the blood is only an indicator of recent exposure.

Animals↗
PubMed1993

Clinical and pathologic findings of blue-green algae (Microcystis aeruginosa) intoxication in a dog.

A healthy dog developed signs of lethargy and vomiting after ingesting water from a tide pool containing blue-green algae. Fulminant hepatic failure occurred, and the dog was euthanized 52 hours later. At necropsy, the liver was large, friable, and discolored a dark red. Histopathology showed hepatocyte dissociation, degeneration, and necrosis. The alga was identified as Microcystis aeruginosa, a known hepatotoxin. The intraperitoneal administration of lyophilized cell material from the bloom caused hepatic necrosis in mice.

Animals↗
PubMedDate not supplied

[Fatal poisoning by water dropwort (Oenanthe crocata)].

The authors relate clinical and toxicological data concerning a recent deadly intoxication by OEnanthe crocata absorption and stress upon awkwardness of clinical diagnosis. Most frequent cases were observed by veterinarians in bovine and porcine intoxications. This plant grows in wet meadows of western France and south-west of England. In spite of its rarity, this intoxication is mostly dangerous and oftenest lethal.

Adult↗
PubMed1980

Treatment of acute carbamazepine intoxication according to its pharmacological properties. Preliminary report.

Acute carbamazepine intoxication represents a pediatric emergency case with symptoms of CNS depression, seizures and water retention. A symptomatic, maintenance treatment is recommended. Taking into account some of the pharmacodynamic properties of this drug (low volume distribution, and antidiuretic activity) we propose a treatment protocol by means of forced diuresis and peritoneal dialysis. This is a preliminary report of the first four cases treated in this way. Objective assessment of intoxication and response to treatment were made based upon urine and blood determinations of the drug. In three cases cure was obtained with a single dose of furosemide; the fourth patient who was critically ill, was dialyzed and improvement was observed 12 hours after. In spite of the reduced number of patients studied, results obtained allow us to conclude that this procedure is advisable in the treatment of carbamazepine intoxication cases.

Acute Disease↗
PubMed1989

[Methods of treating experimental Neguvon poisoning and a comparison of their effects].

The effect of conventional antidotal therapy of oral intoxication due to organophosphorus insecticide Neguvon in male mice is compared to the effect of peritoneal dialysis. As a dialysate, the combination of ACHE reactivator with atropine, distilled water and ACHE preparation has been used. In order to evaluate treatment results, the clinical course of intoxication and the increase of blood ACHE activity inhibited with perorally Neguvon were investigated. The highest increase in activity of inhibited blood ACHE has been stated by the peritoneal dialysis with ACHE preparation. Furthermore, the effects of two dialysates were compared. The first one consisted in ACHE reactivator with atropine, and the second one in ACHE preparation, respectively. The ACHE containing dialysate showed better therapeutical results. The mentioned acetylcholinesterase is stated to be inhibited through the treatment with 50% of Neguvon dosage applied to the experimental animals. Thus the actual dose of Neguvon inducing proper intoxication was reduced to its half amount.

Acetylcholinesterase↗
PubMed1979

Prenatal and postnatal chronic lead intoxication and running wheel activity in the rat.

Prenatal and postnatal chronic lead intoxication was induced in Wistar rats with 0.1 mg/ml PbCl2 in the drinking water of pregnant and lactating females. Offspring were supplied lead water at weaning. Exposure totaled 14 months. Activity was measured in the Wahman LC-33 wheel. Running activity in experimental and control rats was maximized with a 23-hr light cycle followed by a 5-hr dark period in the wheels. There was no significant difference in body weight gains or lead intake (as measured by water consumption) between any sex-matched group. Lead was found to produce overall hypoactivity in both males and females. Under auditory stress the hypoactivity in the males was normalized by combination of a hypoactivity component in the controls and a progressive hyperactivity in the lead animals. This study clearly shows a sex-dependent hypoactivity effect of chronic lead intoxication and suggests its mechanism as an interaction between lead and environmental stress.

Animals↗