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PubMed2004

Changes in the structure and function of the kidney of rats chronically exposed to cadmium. II. Histoenzymatic studies.

Early effects of cadmium (Cd) on the structure and function of the kidney were studied in an experimental model using rats intoxicated with Cd at the levels of 5 and 50 mg Cd/l drinking water. The effect of Cd was evaluated histopathologically and biochemically. Damage to the cellular structures was assessed on the basis of histoenzymatic analyses of the activity and localization of indicator enzymes (succinate dehydrogenase, lactate dehydrogenase, glucose-6-phosphatase, Mg(2+)-dependent adenosine triphosphatase and acid phosphatase). The histochemical observations indicate that Cd causes damage to the organization and function of the nephron. Several structures, i.e. endoplasmic reticulum, mitochondrion, lysosome, cellular and intracellular membrane, as well as their biological functions, i.e. aerobic and anaerobic respiration, transport functions and biochemical processes taking place in the endoplasmic reticulum, were affected. The cytotoxic action of Cd occurs mainly in the tubules and partially also in the glomeruli. The results clearly indicate that Cd damages kidney structurally and functionally even at a relatively low level (5 mg/l) corresponding to human environmental exposure, and they confirm our previous hypothesis that the threshold for the kidney effects of Cd is less than 4.08+/-0.33 microg/g kidney wet weight and higher than 2.40+/-0.15 microg/g. The target for Cd action in the kidney is the tubules (proximal convoluted tubules and straight tubules), and disturbance in their function is the main toxic effect of Cd. Renal glomeruli are also injured, but only partially, whereas in other parts of the nephron the damage is slight. The results, together with observations reported in the first paper of the study, incline us to conclude that humans environmentally exposed to Cd are at risk of tubular damage.

Acid Phosphatase↗
PubMed1980

Lysosomal enhancement in hepatic cells of a teleost fish induced by cadmium.

The toxic effects of cadmium upon the hepatic cells of a freshwater fish were studied. The experiment was developed by the addition of cadmium chloride in the water and histochemical and EM methods were performed. The results showed that acute intoxication induces an increase of lysosomal activity related to the shape, distribution as well as different functional degrees of the organelle condensation. The authors analyze the different situations whose leading alterations of lysosomal behaviour and the probable mechanisms of cadmium action.

Acid Phosphatase↗
PubMed2006

Glutamate and dopamine synaptic terminals in extended amygdala after 14-week chronic alcohol drinking in inbred alcohol-preferring rats.

Alcohol has been shown to affect glutamate (GLU) and dopamine (DA) release and their correlated receptors in the key reward center--extended amygdala--which includes the shell of nucleus accumbens (sNAc) and central nucleus of amygdala (cAmg). It is unclear to date whether there is an alteration in the number of presynaptic GLU/DA nerve terminals. In this study, we investigated the number of GLU and DA terminals in the extended amygdala of alcohol-preferring (P) rats that chronically drank ethanol. P rats have a propensity to drink ethanol to intoxication and develop an alcohol dependency. The P rats were divided into (1) Water group given ad libitum chow and water for 14 weeks; (2) Continuous alcohol group (C-Alc) given ad libitum chow and choice of 15 or 30% (v/v) ethanol or water for 14 weeks; and (3) Repeated deprivation (RD-Alc) group given the same choice of ethanol or water for 6 weeks, followed by a twice repeated cycle of 2 weeks without ethanol followed by 2 weeks with ethanol. Two subpopulations of GLU terminals were labeled by immunostaining for the vesicular GLU transporter 1 (vGLUT1) and vesicular GLU transporter 2 (vGLUT2). DA terminals were labeled by immunostaining for tyrosine hydroxylase (TH). The GLU and DA immunostained (im) varicosities were quantified and analyzed using stereological methods. We found that chronic alcohol did not alter the number of TH-im terminals in the extended amygdala in either the C-Alc or RD-Alc drinking paradigms. Thus, the increases in extracellular levels of DA previously reported following chronic alcohol are likely due to a change in the efficiency of DA release rather than a change in the number of DA terminals. The number of vGLUT1-im terminals was also unchanged in the extended amygdala; however, the number of vGLUT2-im terminals, which represent the greater population of GLU terminals, was increased in the sNAc of the RD-Alc group compared to the Water group. Chronic alcohol is known to affect GLU release, and our findings indicate that repeated alcohol deprivation may preferentially increase GLU terminals in the sNAc bearing the vGLUT2, which are primarily afferents from the thalamus. Our results further indicate that repeated deprivation of alcohol can change the ratio of GLU to DA innervation in the sNAc, a key region of the reward circuitry.

Alcohol Drinking↗
PubMed1984

Toward an analogue of alcoholism in mice: scale factors in the model.

Mice of the C57BL strain, given continuous access to 10% alcohol and plain water, with unlimited food and no stress, frequently drink enough alcohol to produce intoxicating levels in the blood. Nevertheless, this behavior does not appear to replicate the essential features of human alcoholism since the drinking lacks serious toxic effects and the intoxication occurs only as transient episodes in association with homeostatic consumption of fluid and food. It is suggested that continuous monitoring of intake and estimation of the concentration of alcohol in blood, which are now technically feasible, will permit distinction between alcoholic-type drinking and a simple licking for the flavor of alcohol in beverage concentration.

Alcoholism↗
PubMed2002

Low-dose ethanol alters the cardiovascular, metabolic, and respiratory compensation for severe blood loss.

BACKGROUND: Compensation for hemorrhage and shock requires coordination of responses and sufficient physiologic reserve capacity of the cardiovascular, respiratory, renal, and neuroendocrine systems. Intake of ethanol (EtOH) is known to degrade physiologic response to stress. The purpose of this study was to investigate how acute EtOH exposure changes responses to severe blood loss, shock, and resuscitation. METHODS: Conscious male Duncan Hartley guinea pigs were given an intraperitoneal injection of either EtOH (1 g/kg) or an equal volume of water 30 minutes before controlled hemorrhage (60% blood volume), resuscitated after 30 minutes of hypovolemia with a lactated Ringer's solution volume equal to that of the shed blood volume, and observed for 24 hours. Hemodynamic (heart rate, arterial blood pressure), clinical laboratory (arterial blood gases, glucose, lactate, hematocrit), and metabolic gas exchange (oxygen consumption, carbon dioxide production) indicators of shock were monitored. RESULTS: Of the animals that survived 24 hours, changes in arterial pH and lactate were significantly greater in the experiment group than in the control group. Mortality at 24 hours was 77% in the experiment group (EtOH-treated) and 42% (p = 0.39) in the control group (water-treated). CONCLUSION: Acute EtOH exposure, with blood EtOH concentration similar to legal intoxication levels, limits physiologic reserve during hemorrhagic shock and resuscitation. In survivors of shock and resuscitation, compensation is compromised and physiologic reserve is adversely affected by acute EtOH intake.

Alcoholic Intoxication↗
PubMed1982

Accidental deep hypothermia due to exposure.

Two cases of deep hypothermia due to exposure to cold are described. Although the underlying mechanism and degree of hypothermia were comparable, there was a striking dissimilarity between the observed disturbances of body homeostasis, response to rewarming technique, clinical course and outcome in the two cases. The first case was severely acidotic. She was rewarmed by immersion in warm water, but died from an acute cerebrovascular accident. The second case was moderately intoxicated by alcohol and revealed few disturbing features. She was treated by the use of thermal mattresses and survived without complications.

Aged↗
PubMed1989

[Health care of workers engaged in waste water treatment. 1) The exposure conditions to organic solvents in workers engaged in waste water treatment].

In the investigation of the exposure conditions to organic solvents of workers in 35 waste water treatment facilities, it was found that these workers treated various kinds of solvents. Almost all of the facilities treated chloroform, acetone, n-hexane, methanol and carbon tetrachloride. The average exposure concentration of the workers was, however, low. Exposure concentration to organic solvents (chloroform, xylene and carbon tetrachloride) was evaluated in one of the facilities. The average concentration of the respective solvents in the workers did not exceed the threshold limit value of Japan, but the concentration calculated on the basis of combined exposure exceeded the threshold limit value. On the other hand, high concentrations of organic solvents were detected in the room where the solvents were introduced but not in the working rooms, indicating that the workers engaged in waste water treatment were mainly exposed to organic solvents in the former room where they sorted and mixed the solvents and placed them in the incinerator. In conclusion, improvement in working conditions and health care for workers engaged in waste water treatment facilities should be made in order to prevent workers from becoming intoxicated by organic solvents.

Acetone↗
PubMed1983

Optical isomers of 2,3-dimercapto-1-propanesulfonate: antidotal activity, in vitro and in vivo, against sodium arsenite.

DMPS (2,3-dimercapto-1-propanesulfonate, Na salt) is an important water soluble analog of dimercaprol. All investigations of this antidote for heavy metal intoxication have dealt only with the racemic mixture. In the present report, the optical isomers of DMPS have been separated and the arsenic-antidote activity of the levo-rotatory (-)-isomer, the dextro-rotatory (+)-isomer and the racemic mixture of DMPS have been investigated in vivo and in vitro. The individual optical isomers and the racemic mixture of DMPS are effective equally, in vitro, in preventing the inhibition by sodium arsenite of the activity of mouse kidney pyruvate dehydrogenase complex. In addition, when pyruvate dehydrogenase is inhibited, in vitro, by sodium arsenite, any of the three DMPS preparations will reverse the inhibition equally well. The in vitro evidence suggests that two molecules of DMPS are required to prevent the effects of one molecule of sodium arsenite. Neither the LD50 nor the ED50 values of each of the three forms of DMPS differ significantly when measured i.p. in mice. In addition, there is no striking difference between the effectiveness of the levo- or dextro-rotatory DMPS when given orally to mice challenged with sodium arsenite. Thus, the use of the individual optical isomers of DMPS does not appear to have any advantage over the racemic mixture as an arsenic antidote under these conditions.

Administration, Oral↗
PubMedDate not supplied

[Evoluation of biologic balance as a function of radiologic status in a population living in a endemic fluoride zone of southern Algeria].

Chronic fluoride intoxication in subjects living in an endemic South Algerian zone: El Oued (drinking water fluor: 3 to 5 mg/l), provokes some blood and urinary levels modifications, when compared to normals living in Algiers (drinking water fluor: 0,6 mg/l). These modifications are the more often present in stade 0 (normal radiologic aspect) and do not increase with radiological evolution (stades I, II, III). Fluoremy and fluorury increase. Phosphocalcic metabolism is altered. Tubular reabsorption coefficient, particularly, decreases strongly. Using renal functional exploration, a pretty soon tubular failure is founded, which preceeds glomerular failure. Blood levels of certain products and enzymes are studied.

Adolescent↗
PubMed2004

[Concentrations of fluorine, aluminum and magnesium in some structures of the central nervous system of rats exposed to aluminum and fluorine in drinking water].

Fluorine and aluminum are able to pass through the blood-brain barrier and accumulate in the central nervous system (CNS) of exposed animals. Chronic intoxication is accompanied by behavioral disorders, degenerative changes, and abnormalities of aerobic metabolism of the neurons. Awareness of the role of aluminum in Alzheimer's disease stems from epidemiological studies demonstrating increased prevalence of this condition in areas with relatively high content of aluminum in drinking water. The uptake of aluminum in the gastrointestinal tract is decreased in the presence of iron, calcium, magnesium, phosphate, or fluoride. Many magnesium-containing enzymes are affected by aluminum, which is able to replace magnesium and thus reduce their activity. The purpose of this study was to determine the concentrations of fluorine, aluminum, and magnesium in some structures of the CNS of rats exposed to fluorine and aluminum in water. Our material consisted of 64 Wistar rats divided into eight equal groups. Groups I, II and III were female rats exposed, respectively, to 100 ppm fluorine ions, 300 ppm aluminum ions or both at same doses alternating every second day. Groups IA, IIA and IIIA consisted of male rats exposed like the respective female groups. Control groups K1--females and K2--males received distilled water ad libitum. Exposure lasted 31 days whereupon the animals were anesthetized with ketamine and sacrificed. The brain was collected and the cerebellum, brain cortex, and hippocampus were isolated. Concentrations of fluorine, aluminum, and magnesium were measured with prior mineralization of wet tissues in a microwave oven. Fluorine concentrations were determined with a potentiometric method and ion-selective electrode. Aluminum was measured with ICP (inductively coupled plasma) and magnesium with ASA (atomic absorption spectrometry). The highest concentrations of fluorine were observed in rats exposed to fluorine only. The same pattern was true for aluminum. Groups exposed alternatively to both elements demonstrated lower accumulation of fluorine whereas accumulation of aluminum did not change significantly. Apparently, aluminum reduced the availability of fluorine but there was no reciprocal effect. No significant changes in the concentrations of magnesium were noted, regardless of the brain structure or group. It can thus be concluded that exposure to fluorine, aluminum or both has little effect on the concentration of magnesium in the CNS of rats.

Aluminum↗
PubMed2000

[Lavage almost never indicated after an autointoxication].

In many Dutch hospitals gastric lavage leaving charcoal and a laxative is the treatment of choice after autointoxication. Gastric lavage is not without risks. No difference has been demonstrated in efficacy and safety of gastric lavage combined with administration of activated charcoal on the one hand and just administration of activated charcoal on the other. In theory, gastric lavage might be useful in patients presenting shortly after the selfpoisoning (up to 2 hours) and in the case of delayed gastric emptying up to 4 hours. Gastric lavage is indicated without doubt in patients presenting shortly after ingestion of toxic substances which are poorly adsorbed by charcoal (for instance lithium). In case of a mild intoxication (for example with benzodiazepines), the risks of drug toxicity do not outweigh those of lavage, regardless of the time elapsed after ingestion. If gastric lavage is applied, it should be performed properly, i.e. with warm water (38 degrees C), with a 36-40 Fr. tube, using aliquots of 200-300 ml. In a minority of the intoxications whole bowel lavage should be employed.

Charcoal↗
PubMed1983

Falsely high serum creatinine concentration associated with severe methanol intoxication.

A case of severe methanol intoxication (1300 mg/L) was associated with markedly increased serum creatinine (490 mg/L) despite normal urea values and the absence of any other signs of renal disease. These values declined progressively to normal, and the patient recovered with no visual impairment. Additional laboratory experimentation suggested that the high creatinine value was probably ascribable to some unknown foreign material(s) in the patient's blood that reacted with the alkaline picrate used in the measurement of creatinine. One of the presumed metabolites of methanol, formaldehyde, reacts with creatinine but the product does not react with picrate. We believe that the foreign material was derived from either commercial preparations of methanol or contaminants in the patient's drinking water.

Alcoholic Intoxication↗
PubMed1990

Histopathological lesions in the body organs of cat-fish (Heteropneustes fossilis) following mercury intoxication.

Light microscopic study of different body organs of cat-fish following exposure to HgCl2 0.2 mg/L in water for 30 days revealed that focal degeneration of liver cells and disorganization of hepatic cords occurred at places. Furthermore, centrilobular atrophy and compensatory hypertrophy of some hepatic cells were also observed. In the kidneys disintegration of renal epithelium along with displacement of nuclei, shrinkage of glomeruli, breakdown of Bowman's capsule and heavy infiltration by inflammatory cells were observed. The histopathological changes noted in the intestine included degeneration of lining epithelium, and diminution of goblet cells. Microscopic section of ovaries exhibited reduction of ooplasm leading to formation of atypical oocytes. An increase in the occurrence of atretic oocytes and interfolicular spaces was also discernible. No histopathological lesions could be detected in testes of male fish probably because of the difference in the maturity of the control and experimental groups. The pathomorphological alterations in relation to mercury toxicity in spleen were associated with the disorganization of the splenic cords resulting in the displacement of lymphatic tissue cells within the substance of splenic pulp. Marked depletion of the red pulp was noticeable.

Animals↗
PubMed1992

Osteochondral lesions in developing rats intoxicated with thallium twenty four hours after birth.

An i.p. injection of a solution of thallium acetate in deionized water at a dose of 32 mg/kg, in 24-h-old rats, produces morphological and biochemical alterations in both cartilaginous and osseous tissues. From the beginning, there are alterations in the cartilaginous cell as well as in chrondrine, osteoblasts, osseous tissue and bone marrow. Rats were sacrificed at 24, 48, and 72 h and also at 7 days. Two animals survived for 50 days. One showed total irreversible alopecia while the other one had partial alopecia with discrete recovery. Both showed a low weight and a size of 8 cm. Microscopically, degenerative changes were produced consisting of alteration and death of many cartilaginous cells, uneven metachromasia and the chondrine and decrease of the growth cartilage, scanty bone trabeculae with few osteoblasts. The bone marrow showed few myeloblasts and megakaryocytes. Progressive cellular damage throughout the 50 days of survival represents a response of the thallium ionic accumulation and recycling in cellular mitochondria of all the body's cells. This appeared in our study as irreversible and progressive osteochondral alterations with atrophy of the skin and its adnexa, hyalinization of elastic and collagenous fibers with intense interstitial edema.

Alopecia↗
PubMed1987

Cardiovascular responses to face immersion (the diving reflex) in human beings after alcohol consumption.

The diving reflex is a complex cardiovascular-respiratory response to immersion. This multireflex response in animals consists of apnea; bradycardia (the experimental parameter most often measured); peripheral vasoconstriction (resulting in preferential perfusion of the brain and heart); decreased cardiac output (with a maintained or increased stroke volume); and an increase in mean arterial blood pressure. These cardiovascular alterations act in a manner that conserves oxygen for the heart and brain. Because alcohol is often involved in water accidents with associated submersions, these initial experiments dealt with human volunteers who consumed alcohol to a blood level of 0.1 g% (legal level of intoxication). The diving reflex was elicited before and after alcohol consumption. Heart rate, blood pressure, and cardiac output were measured before, during, and after face immersion in 4 C water. In the sober state, immersion decreased heart rate, increased stroke volume, increased blood pressure, and increased total peripheral resistance. In comparison to the sober state, alcohol consumption increased pre-immersion heart rate, but did not significantly alter pre-immersion blood pressure or stroke volume. Following alcohol consumption, facial immersion decreased heart rate, but not to the same low rate as in the sober state. Alcohol consumption also evoked a lesser increase in blood pressure and failed to increase stroke volume significantly.

Adult↗
PubMedDate not supplied

The role of cernitins in cadmium effect on the absorption processes in rat small intestine.

The effect of long-term intoxication of cadmium (administered subcutaneously in a dose of 1 mg Cd/kg of body weight once a week for one month) on the absorption of water, sodium, potassium, glucose, glycine and thiamine in the small intestine of rats was investigated. In addition, the influence of cernitins (special pollen extract) on the action of cadmium intoxication was tested. The cernitins were given by stomach pump in the form of an aqueous solution of Pollitabs Sport tablets in a dose of 1.5 mg of cernitin T-60 and 0.075 mg of cernitin GBX per individual twice a week for two weeks or four weeks according to the group of animals tested. The results indicated that long-term administration of cadmium increased the intestinal absorption of all tested substances. Meanwhile, the application of cernitins reduced the effects of cadmium intoxication upon intestinal absorption and the processes of absorption was close to normal.

Animals↗