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PubMed1983

Effect of body temperature on salicylate-induced hyperventilation.

Hyperventilation and hyperpyrexia occur simultaneously during acute salicylate intoxication. The present experiments were designed to investigate the stimulatory effect of increased body temperature on respiration in this pathological state. Acute salicylate intoxication was produced in mongrel dogs by intravenous infusion of 200 mg sodium salicylate/kg body weight, and the effect of body temperature on salicylate-induced hyperventilation was studied by comparing the respiration of hyperthermic animals with the respiration of animals maintained normothermic during acute salicylate intoxication by bathing them in cold water. The minute volume of ventilation increased greatly over control levels in both normothermic and hyperthermic animals, but this increment was much larger in hyperthermic animals. The increase in ventilation of normothermic animals can be explained as a rise in alveolar ventilation which results in hypocapnia despite large increases in carbon dioxide production and oxygen consumption during acute salicylate intoxication. The further augmentation of ventilation in hyperthermic animals can be explained as a rise in deadspace ventilation in response to increased body temperature during acute salicylate intoxication.

Animals↗
PubMed1984

[Weight increase and chronic experimental poisoning by tobacco smoke in the albino rat. Effect of protection with mineral waters].

The Authors refer to the results of an experiment conducted on albino rats chronically intoxicated with tobacco smoke. Several groups of animals were contemporaneously protected, by drinking or by inhaling or by both methods, by a beneficial sulphureous water with a varying sulphydrometric degree, and in one experiment, by inhaling a hypertonic salso-bromo-iodic water. In all cases, it was possible to observe that in the adopted experimental conditions, the chronic intoxication from tobacco smoke slowed the weight increase of albino rats subjected to intoxication and not protected, both as regards non-intoxicated animals and as regards intoxicated animals protected by one of the studied waters. There were no statistically significant differences between the weight increase of the animals protected by the drinking or inhaling methods while protection via both methods resulted statistically more efficacious than protection by one single method.

Animals↗
PubMed2005

Hepatoprotective effect of green tea (Camellia sinensis) extract against tamoxifen-induced liver injury in rats.

Tamoxifen citrate (TAM), is widely used for treatment of breast cancer. It showed a degree of hepatic carcinogenesis. The purpose of this study was to elucidate the antioxidant capacity of green tea (Camellia sinensis) extract (GTE) against TAM-induced liver injury. A model of liver injury in female rats was done by intraperitoneal injection of TAM in a dose of 45mg Kg(-1) day(-1), i.p. for 7 successive days. GTE in the concentration of 1.5 %, was orally administered 4 days prior and 14 days after TAM-intoxication as a sole source of drinking water. The antioxidant flavonoid; epicatechin (a component of green tea) was not detectable in liver and blood of rats in either normal control or TAM-intoxicated group, however, TAM intoxication resulted in a significant decrease of its level in liver homogenate of tamoxifenintoxicated rats. The model of TAM-intoxication elicited significant declines in the antioxidant enzymes (glutathione-S-transferase,glutathione peroxidase, superoxide dismutase and catalase) and reduced glutathione concomitant with significant elevations in TBARS (thiobarbituric acid reactive substance) and liver transaminases; sGPT (serum glutamate pyruvate transaminase) and sGOT (serum glutamate oxaloacetate transaminase) levels. The oral administration of 1.5 % GTE to TAM-intoxicated rats, produced significant increments in the antioxidant enzymes and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases levels. The data obtained from this study speculated that 1.5 % GTE has the capacity to scavenge free radical and can protect against oxidative stress induced by TAM intoxication. Supplementation of GTE could be useful in alleviating tamoxifen-induced liver injury in rats.

Animals↗
PubMed2002

Effects of ascorbic acid and alpha-tocopherol on arsenic-induced oxidative stress.

Arsenic is an ubiquitous element in the environment causing oxidative burst in the exposed individuals leading to tissue damage. Antioxidants have long been known to reduce the free radical-mediated oxidative stress. Therefore, the present study was designed to determine whether supplementation of alpha-tocopherol (400 mg/kg body weight) and ascorbic acid (200 mg/kg body weight) to arsenic-intoxicated rats (100 ppm in drinking water) for 30 days affords protection against the oxidative stress caused by the metalloid. The arsenic-treated rats showed elevated levels of lipid peroxide, decreased levels of non-enzymatic antioxidants and activities of enzymatic antioxidants. Administration of alpha-tocopherol and ascorbic acid to arsenic-exposed rats showed a decrease in the level of lipid peroxidation (LPO) and enhanced levels of total sulfhydryls, reduced glutathione, ascorbic acid and alpha-tocopherol and so do the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase to near normal. These findings suggest that alpha-tocopherol and ascorbic acid prevent LPO and protect the antioxidant system in arsenic-intoxicated rats.

Administration, Oral↗
PubMed1975

Changes in intracranial pressure and brain hydration during acute ethanolism.

Intracranial hypertension and brain hydration were scrutinized during acute ethanolism for consideration in the combined head injury setting. Intraventricular pressures and whole brain water levels rose with moderate or high ethanol dosages. The most prominent alterations were associated with respiratory acidosis and hypoxia; less marked changes were found in their absence and point to a second mechanism. Elevated central venous pressures appeared as well in some instances to constitute a third action. It is accordingly suggested that ethanol may add significantly to the combined pathology with associated acute head injury in several ways. These include: contributions to edema formation, to respiratory depression, and to alterations in local hemodyamics.

Alcoholic Intoxication↗
PubMed2000

The calculation of blood ethanol concentrations in males and females.

In German-speaking countries, blood ethanol concentrations (BECs) are usually calculated using Widmark's equation. The distribution factor r of this equation is a correction factor needed to obtain a reduced body mass and corresponds to the ratio of total body water and blood water content. To enhance the reliability of Widmark's model equation, the body weight, body height, blood water content and total body water of 256 women and 273 men were measured. The ratio of body water to blood water ranged from 0.44 to 0.80 in women and from 0.60 to 0.87 in men. For both sexes equations were developed by multiple regression analysis which allow the determination of the individual, more realistic distribution factors rFI (for females) and rMI (for males) even when only body height and body weight are known. Drinking experiments revealed a clearly higher congruence of calculated and measured blood ethanol concentrations when rFI or rMI were used instead of rigid distribution factors, i.e. 0.6 for women and 0.7 for men with or without the assumption of a 10% so-called resorption deficit. Additionally, Widmark's equation in combination with rFI or rMI allows a more accurate prediction of blood ethanol concentrations than the equations of Watson and Ulrich.

Adult↗
PubMed1981

Kidney morphology and function in lithium-treated patients.

The findings of morphological changes in the kidneys of some patients given long-term treatment with lithium and indications that lithium intoxications frequently are preceded by alterations in water and electrolyte metabolism have generated new interest in the effect of long-term lithium treatment on kidney structure and function. Today it is not firmly established to which extent renal morphological changes are present in unselected groups of patients given long-term treatment with lithium. Neither is it clear what is the clinical significance of these changes and what are the relative roles played by lithium, concomitant and previous treatment with other psychotropic drugs, previous occurrence of lithium intoxications, and coexistence of somatic illness for their development. Studies on kidney function in long-term lithium-treated patients, however, have revealed that affection of GFR was either moderate or absent indicating that the risk of renal insufficiency and terminal azotemia is remote even when lithium is given for many years. A large number of patients have altered water excretion with polyuria or lowered urine concentrating ability or both. Due to the extra fluid loss these patients are apt to develop dehydration, and they may then be in danger of lithium intoxication. We hypothesize that lithium-induced changes of kidney function may become less frequent and less pronounced if patients are maintained at serum lithium levels somewhat lower (0.5-0.8 mmol/l) than those commonly employed. We recommend careful monitoring of serum lithium levels, regular control of kidney function, and extra caution when physical illness or additional drug treatment may lead to disturbance of fluid and electrolyte balance.

Glomerular Filtration Rate↗
PubMedDate not supplied

Discrimination between different types of white matter edema with diffusion-weighted MR imaging.

Brain edema can be classified into three categories: vasogenic, cytotoxic, and interstitial. The mechanism of edema is thought to be different in each type. The authors studied the movement of water molecules in each type of white matter edema in a rat model by using diffusion-weighted magnetic resonance imaging. Conventional T2-weighted imaging did not allow distinction between the three types of white matter edema; the three types of edema were, however, distinguished by using diffusion-weighted imaging. The apparent diffusion coefficient (ADC) of water was different in each type of edema. Water molecules in cytotoxic edema induced by triethyl-tin intoxication showed a smaller and less anisotropic ADC than in normal white matter. In contrast, water in vasogenic edema induced by cold injury had a larger and more anisotropic ADC than in normal white matter. Water in interstitial edema due to kaolin-induced hydrocephalus had an anisotropic and very large ADC.

Animals↗
PubMed2003

Changes in the structure and function of the kidney of rats chronically exposed to cadmium. I. Biochemical and histopathological studies.

The aim of this study was to assess the effects of chronic exposure to cadmium (Cd) on the structure and function of kidneys, as well as to establish the body burden of Cd at which the changes occur. For this purpose we have created an experimental model using rats intoxicated with Cd administered in drinking water at the concentration of 5 or 50 mg Cd/l for 6, 12 and 24 weeks. The degree of kidney damage was evaluated biochemically and histopathologically. Sensitive biomarkers of Cd-induced proximal tubular injury such as urinary total N-acetyl-beta- d-glucosaminidase (NAG-T) and its isoenzyme B (NAG-B), and alkaline phosphatase (ALP) were used. Cd content in the kidney increased with the level and duration of exposure leading to dose- and time-dependent structural and functional renal failure. In rats exposed to 5 mg Cd/l, first symptoms of injury of the main tubules of long and short nephrons (structural damage to epithelial cells, increased urinary activities of NAG-T and NAG-B) were noted after 12 weeks of the experiment. The damage occurred at a low kidney Cd concentration amounting to 4.08+/-0.33 micro g/g wet weight (mean +/-SE) and a urinary concentration of 4.31+/-0.28 micro g/g creatinine. On exposure to 50 mg Cd/l, damage to the main tubules (blurred structure of tubular epithelium, atrophy of brush border, partial fragmentation of cells with release of nuclei into tubular lumen as well as increased urinary activities of NAG-T, NAG-B and ALP) was already evident after 6 weeks with the kidney Cd concentration of 24.09+/-1.72 micro g/g wet weight. In rats exposed to 50 mg Cd/l, a lack of regular contour of glomeruli was noted after 12 weeks, whereas after 24 weeks thickening of capillary vessels and widening of filtering space were evident. After 24 weeks of exposure to Cd, increased urea concentration in the serum with simultaneous decrease in its level in the urine, indicating decreased clearance of urea, and increased excretion of total protein were observed, but endogenous creatinine clearance remained unaffected. At the lower exposure, symptoms of structural, but not functional, damage to the glomeruli were also evident after 24 weeks of the experiment. Our results provide evidence that chronic exposure to Cd dose-dependently damages (structurally and functionally) the whole kidney. The injury affects the main resorptive part (proximal convoluted tubules and straight tubules) and the filtering part (glomeruli) of the nephron. But the target site for Cd action is the main tubule. We hypothesize that the threshold for Cd effects on the kidney is less than 4.08+/-0.33 micro g/g wet kidney weight and greater than 2.40+/-0.15 micro g/g (at this Cd concentration no symptoms of kidney damage were noted), and it may be close to the latter value. A very important finding of this study is that Cd acts on the whole kidney, especially on the main tubules, even at relatively low accumulation in this organ. It confirms the hypothesis that humans environmentally exposed to Cd, especially smokers, are at risk of tubular dysfunction.

Acetylglucosaminidase↗
PubMed2003

Effects of chronic exposure to cadmium on renal cytochrome P450-dependent monooxygenase system in rats.

The aim of this study was to evaluate the effects of chronic exposure to cadmium (Cd) on the renal cytochrome P450-dependent monooxygenase system. For this purpose, male Wistar rats were intoxicated with Cd administered in drinking water at a concentration of 5 or 50 mg Cd/l for 6, 12 and 24 weeks. Concentrations of cytochrome P450 and cytochrome b(5) as well as activities of NADPH-cytochrome P450 reductase and NADH-cytochrome b(5) reductase were determined in the kidney microsomal fraction. Protein content of CYP1A1, CYP2E1 and CYP3A1 cytochrome P450 isoforms was evaluated as well. In the rats exposed to 5 mg Cd/l, the concentration of cytochrome P450 decreased (by 41%) after 24 weeks of the experiment. The activity of NADPH-cytochrome P450 reductase decreased (by 24%) after 6 and 12 weeks, whereas after 24 weeks it remained unchanged, compared with the control group. Moreover, a decrease in the concentration of cytochrome b(5) (by 25, 15 and 26% at 6, 12 and 24 weeks, respectively) and the activity of its NADH reductase (by 26 and 31% at 6 and 24 weeks, respectively) was noted in these animals. At the exposure to 50 mg Cd/l, the concentrations of cytochrome P450 and cytochrome b(5) and the activities of their corresponding reductases were decreased at each time-point. Western blot analysis revealed that all isoforms of cytochrome P450 studied were affected by Cd and the effect was dependent on the level and the duration of exposure. The results of this study indicate that chronic exposure to Cd in a dose- and time-dependent manner affects the kidney cytochrome P450-dependent monooxygenase system by decreasing the concentrations of cytochrome P450 and cytochrome b(5) and inhibiting the activities of their corresponding reductases. The effect of Cd on the cytochrome P450 content is associated with its ability to stimulate or inhibit of various P450 isoforms. A very important finding of this study is that Cd affects the kidney cytochrome P450-dependent monooxygenase system at relatively low exposure and low kidney Cd accumulation (2.40+/-0.15 microg/g). As the experimental model used reflects human exposure to Cd, we conclude that Cd can affect the kidney cytochrome P450-dependent monooxygenase system in environmentally exposed humans. Previously we have reported disorders in the system in the liver of rats at the same levels of exposure as in this study. Thus, we hypothesize that the metabolism and detoxification of many substances, including xenobiotics, may be seriously affected in Cd-exposed subjects.

Administration, Oral↗
PubMed1995

Severe hypercalcemia and polyuria in a near-drowning victim.

A 73-year-old man was admitted because of near-drowning in a hot springs bath. Transient severe hypercalcemia and polyuria were seen during the first hospital day. It seemed that the hypercalcemia was due to acute intoxication from calcium contained in the water of the spring absorbed mainly through the alveoli. To our knowledge, this is the first case of acute hypercalcemia complicating a near-drowning in a hot spring. Analysis of serum and urine electrolytes during the polyuric phase revealed saline diuresis, which was probably due to interference by the hypercalcemia of the reabsorption of sodium and free water.

Aged↗
PubMedDate not supplied

[Pseudomigraine as a symptom of carbon monoxide intoxication].

INTRODUCTION: Carbon monoxide poisoning (CO) is a common intoxication. Diagnosis is sometimes difficult since the symptoms may be very varied. We report a case of repeated intoxication which led to several consultations and admission to hospital, since there were headaches and loss of consciousness suggesting basilar migraine. CASE REPORT: A 30 year old woman consulted for repeated headaches over the previous six months, normally occurring in the morning, accompanied by vertigo, nausea and vomiting and loss of consciousness on two occasions. Clinical examination and the complementary tests done (laboratory analysis, cerebral MR, ECG, ECG Holter, EEG) were normal. Finally CO intoxication was diagnosed when levels of carboxyhemaglobin of over 30% were found in both the patient and her sister. The cause was a faulty water heater, confirmed on technical inspection. CONCLUSIONS: CO intoxication may present as repeated headaches, with or without alteration in consciousness. Finding similar symptoms in other people living in the same place should increase suspicion. In certain case, anamnesis should include details regarding apparatus used for heating, cooking and bathrooms. More carboxyhaemaglobin estimations should be done in Emergency Departments.

Adult↗
PubMed2002

Rabbitfish ("aras"): an unusual source of ciguatera poisoning.

BACKGROUND: Ciguatera poisoning is the commonest fish-borne seafood intoxication. It is endemic to warm water tropical areas and is caused by consumption of bottom-dwelling shore reef fish, mostly during spring and summer. The causative agent, ciguatoxin, is a heat-stable ester complex that becomes concentrated in fish feeding on toxic dinoflagellates. The common clinical manifestations are a combination of gastrointestinal and neurologic symptoms. Severe poisoning may be associated with seizures and respiratory paralysis. OBJECTIVE: To describe a series of patients who sustained ciguatera poisoning in an uncommon region and from an unexpected source. PATIENTS: Two families complained of a sensation of "electrical currents," tremors, muscle cramps, nightmares, hallucinations, agitation, anxiety and nausea of varying severity several hours after consuming rabbitfish ("aras"). These symptoms lasted between 12 and 30 hours and resolved completely. The temporal relationship to a summer fish meal, the typical clinical manifestations along with the known feeding pattern of the rabbitfish suggested ciguatera poisoning. CONCLUSIONS: The Eastern Mediterranean basin is an unusual region and the rabbitfish an unusual source for ciguatera poisoning. There are no readily available and reliable means for detecting ciguatoxin in humans. A high index of suspicion is needed for diagnosis and a thorough differential diagnosis is essential to eliminate other poisonings, decompression sickness and encephalitis. Supportive therapy is the mainstay of treatment.

Adult↗
PubMedDate not supplied

[Chronic arsenic poisoning].

A case of chronic arsenic intoxication due to ingestion of contaminated water for several years is reported. The main symptoms were keratosis palmaris et plantaris, confetti - Like dyschromias in chest, post - necrotic liver cirrhosis multiple intraepithelial epidermoid carcinomas and invasive epidermoid carcinoma. The epidemiologic study showed high concentration of arsenic in the water of the well used by the patient; likewise, chronic arsenicalism was found in the whole family and in several neighbors who consumed water from the same well.

Adolescent↗
PubMed1985

[Alcohol dehydrogenase in the blood and liver of rats with different alcoholic motivation].

Alcohol dehydrogenase (ADH) activity was determined by a highly sensitive method. The enzyme activity in the blood serum was similar in alcohol and water preferring rats, while ADH activity in the liver of alcohol preferring rats was higher than in water preferring rats. In rats, chronically intoxicated with ethanol, ADH activity in the liver decreased, while in the serum it was twice higher than the normal level. It is suggested that high level of blood ADH is not connected with the rate of enzyme synthesis in the liver.

Alcohol Drinking↗
PubMed1993

[Histochemical estimation of zinc accumulation in hepato-pancreatic gland cells of the snail Lymnaea stagnalis (L.)after subacute poisoning with zinc acetate considering infection with Digenea larvae].

Accumulation of zinc in epithelial cells of the digestive gland tubules of the fresh-water snail Lymnaea stagnalis after subacute intoxication with zinc acetate (strong increasing doses of the metal in short period of time) was histochemically examined using dithizone. Large zinc granules observed in medial and basal parts of calcium cells permitted to conclude that this metal is bound in cytoplasm mainly on granules built of calcium and magnesium phosphate. There were no smaller concentrations of zinc, that would be indicative for metal binding with cytoplasmatic metallothionein-like proteins. In calcium cells of the digestive gland tubules of snails infected with Digenea larvae accumulation of zinc was stronger, that would be an aspect of compensatory reaction.

Acetates↗