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PubMed1999

Lead intoxication: antioxidant defenses and oxidative damage in rat brain.

Oxidative damage associated with the presence of lead (Pb) in the brain has been proposed as one possible mechanism involved in Pb toxicity. To investigate this hypothesis, we examined the long-term effects of Pb2+ on parameters of oxidative stress in the brain from rats chronically exposed to the metal (1 g Pb acetate/1 drinking water). After 8 weeks of treatment, Pb2(+)-intoxicated rats (blood Pb concentration > 100 microg/dl) showed lower body weight, and lower hematocrit and 5-aminolevulinic acid dehydratase activity as compared to controls. The content of brain 2-thiobarbituric acid-reactive substances (TBARS), an indicator of lipid oxidation, was significantly (P < 0.05) higher in the Pb2(+)-intoxicated animals than in controls. Higher activities of the antioxidant enzymes glutathione reductase and glutathione peroxidase, and a lower (44%) level of ubiquinol 10 were found in the brain of the Pb2(+)-treated rats, compared to controls. A negative correlation between brain ubiquinol 9 (r2 = 0.79), 10 (r2 = 0.84) and blood Pb concentration was observed. Brain alpha-tocopherol levels, superoxide dismutase activity and parameters of oxidative damage to proteins were similar between control and Pb2(+)-treated rats. The present results indicate that chronic Pb2+ intoxication induces an oxidative stress situation in rat brain.

Animals↗
PubMed1985

Intracellular accumulation of mercury in the anterior pituitary of rats exposed to mercuric chloride.

A histochemical technique has been used to reveal mercury deposits by light and electron microscopy in the anterior pituitary of adult rats. After administration of mercuric chloride either in the drinking water or by intraperitoneal injection, deposits were found within lysosomes and secretory granules in somatotrophs, thyrotrophs, follicular cells, and marginal cells. The amount of mercury deposited was proportional to the dose of mercuric chloride given. Significantly more mercury was found in rats given intraperitoneal injections compared to those intoxicated with mercuric chloride in the drinking water. Mercury was retained in the cells for at least 4 months after the last injection although the amount of deposits decreased in this period.

Animals↗
PubMed2006

Cadmium: cellular effects, modifications of biomolecules, modulation of DNA repair and genotoxic consequences (a review).

Cadmium is an important toxic environmental heavy metal. Occupational and environmental pollution with cadmium results mainly from mining, metallurgy industry and manufactures of nickel-cadmium batteries, pigments and plastic stabilizers. Important sources of human intoxication are cigarette smoke as well as food, water and air contaminations. In humans, cadmium exposures have been associated with cancers of the prostate, lungs and testes. Acute exposures are responsible for damage to these organs. Chronic intoxication is associated with obstructive airway disease, emphysema, irreversible renal failure, bone disorders and immuno-suppression. At the cellular level, cadmium affects proliferation, differentiation and causes apoptosis. It has been classified as a carcinogen by the International Agency for Research on Cancer (IARC). However, it is weakly genotoxic. Indirect effects of cadmium provoke generation of reactive oxygen species (ROS) and DNA damage. Cadmium modulates also gene expression and signal transduction, reduces activities of proteins involved in antioxidant defenses. Several studies have shown that it interferes with DNA repair. The present review focuses on the effects of cadmium in mammalian cells with special emphasis on the induction of damage to DNA, membranes and proteins, the inhibition of different types of DNA repair and the induction of apoptosis. Current data and hypotheses on the mechanisms involved in cadmium genotoxicity and carcinogenesis are outlined.

Cadmium↗
PubMed1989

Detection of the early steps of cadmium nephropathy--comparison of light- and electron-microscopical patterns with the urinary enzymes excretion. An experimental study.

Few data are yet available comparing the histological patterns of cadmium nephropathy with the values of urinary enzyme excretions, useful indexes of renal tubular damage. 40 Wistar rats, divided into four groups (A-D), were intoxicated with cadmium chloride (CdCl2) at 16 ppm in drinking water for 4, 16, 40 and 60 weeks, respectively. At the end of each period all the intoxicated rats and 5 controls were assessed for creatinine clearance, fractional excretion of gamma-glutamyltransferase (UfrGGT) and alpha-glucosidase (UfrAGL), indexes of anatomical tubular damage, and for fractional clearance of lysozyme (CfrLys), index of functional tubular damage. Thereafter, the rats were sacrificed and their kidneys examined with light and electron microscopy. Control rats and group A and B rats did not show any histological impairment. A widespread vesiculation of proximal tubular cells with mitochondrial and lysosomal alterations was found in the group C rats and was more evident in group D. The brush border never showed any damage in all groups in accordance with the finding of a normal excretion pattern of UfrGGT, an enzyme situated in this structure. The UfrAGL was increased only in group D rats (p less than 0.025), who showed the most severe anatomical damages. The CfrLys, an index of tubular function, was elevated in group C and D rats (p less than 0.02 and p less than 0.002, respectively). It was possible to detect the initial renal tubular damage.

Animals↗
PubMed2005

Preventive action of green tea from changes in the liver antioxidant abilities of different aged rats intoxicated with ethanol.

OBJECTIVE: The present study investigated the influence of green tea as a source of water-soluble antioxidants on the liver antioxidant potential of different aged rats chronically intoxicated with ethanol. METHODS: Rats (2, 12, and 24 mo old) were fed for 5 wk on a control or an ethanol Lieber-DeCarli diet with and without green tea (7 g/L). The activity and level of enzymatic and non-enzymatic antioxidants and the level of markers of protein and lipid oxidation in the liver of rats were examined. RESULTS: The activities of superoxide dismutase and catalase and levels of vitamins C, E, A, and beta-carotene were significantly decreased, whereas activities of glutathione peroxidase and glutathione reductase and the level of reduced glutathione significantly increased during aging. The ethanol diet caused a significant decrease in activity of antioxidant enzymes and in the level of non-enzymatic antioxidants tested. Administration of green tea to ethanol-treated rats of different ages partly normalized the activity of enzymes and the level of non-enzymatic antioxidants. Changes in antioxidant ability observed during aging were accompanied by increased levels of markers of lipid and protein modifications that also were intensified by ethanol. Green tea caused a decrease in lipid and protein oxidation in aged and ethanol-treated rats. The protective effect of green tea was confirmed by the significantly lower activity of biomarkers of liver damage (alanine and aspartate aminotransferases) in the serum of rats that received green tea with ethanol compared with rats from the control ethanol group. CONCLUSIONS: The use of green tea appears to be beneficial to rat liver by decreasing oxidative stress caused by ethanol and/or aging.

Age Factors↗
PubMed1990

[Effects of inmecarb on alcohol intake and the state of hepatic cytochrome P-450 system during various stages of experimental alcoholism in rats].

The influence of the new anti-alcohol drug Inmecarb on the alcohol consumption as well as on activity of the liver cytochrome P-450 system was studied in rats during chronic alcohol intoxication in the free choice situation between water and 15% ethanol solution. It was shown that voluntary alcohol consumption of different duration (10 days to 8 months) does not change the activity of liver cytochrome P-450 system. Inmecarb treatment (40 mg/kg, i.p. twice a day) during 14 days resulted in decrease of alcohol consumption in rats. This effect was most pronounced in late stages of experimental alcoholism. Inmecarb decreases the cytochrome P-450 content and suppresses the activity of aniline hydroxylase in rats with different duration of voluntary alcohol intoxication, but most pronounced effect was observed during the late stages of experimental alcoholism.

Alcohol Drinking↗
PubMed1985

Acute alcohol intoxication and body composition in women and men.

The present study was a direct experimental comparison of administering equivalent alcohol doses based on body weight and estimated total body water to 12 women and 12 men. Each subject participated in two experimental sessions separated by at least three days. Two doses of 95% ethanol were administered in a randomized, counterbalanced order: 0.66 ml/kg of body weight, and 1.2 ml/l of total body water. Women were tested during the midfollicular phase of their menstrual cycle when plasma concentrations of estrogen and progesterone have been found to be lower than other phases of the cycle. When given doses equated for body weight, women reached significantly higher peak blood alcohol concentrations than men. No sex differences were found when equivalent doses based on total body water were administered. This differential effect of dose determination was not reflected in self-reported levels of alcohol intoxication. The anthropometric equations used to estimate total body water provided a practical, reliable method for equating alcohol doses.

Adult↗
PubMed1988

Acute zinc intoxication: comparison of the antidotal efficacy of several chelating agents.

Four zinc compounds (acetate, nitrate, chloride and sulfate) were administered po or ip to rats and mice. The LD50 values were determined. Animals were observed for 14 days. The majority of deaths occurred during the first 48 hr. The clinical and physical signs appearing after intoxication included miosis, conjunctivitis, decreased food and water consumption and hemorrhages and hematomas in the tail. These changes decreased with time which would suggest a quick elimination of zinc. To determine the effect of 6 chelating agents on the toxicity of zinc, various doses of zinc acetate (66-330 mg/kg) were given ip to male mice followed by the injection of one of the chelators. DTPA, D-PA, CDTA and EDTA were the most effective. CDTA and DTPA were also the most effective in increasing the urinary excretion of zinc. DTPA appears to be the most effective agent of those tested in the prevention of acute zinc intoxication. However, CDTA may be considered as a possible alternative.

Animals↗
PubMed1986

Antagonism of dithiobiuret toxicity in rats.

Daily administration of dithiobiuret (DTB, 1 mg/kg X 6 days, ip) produced delayed onset muscle weakness in rats as indicated by failure in a treadmill test. In nerve-muscle preparations from DTB-intoxicated rats neuromuscular toxicity was manifested as contractile fatigue during tetanic nerve stimulation. As muscle weakness developed, feed intake decreased and the animals lost body weight. Water intake was not altered during this time, but urine output was increased concomitant with the development of muscle weakness and resulted in a state of negative water balance. Daily administration of d-penicillamine (d-PEN) antagonized DTB-induced treadmill failure in a dose-dependent fashion. A daily dose of d-PEN (1 mMol/kg, ip) that completely antagonized treadmill failure also antagonized the contractile fatigue, reduced feed intake, weight loss and negative water balance caused by DTB administration. In rats already intoxicated with DTB, initiating daily d-PEN treatment or discontinuing further DTB administration, caused the animals to recover normal treadmill performance after a latent period of five days. A single dose of d-PEN (1 mMol/kg, iv) was not effective in reversing treadmill failure or contractile fatigue in rats already intoxicated with DTB. Thus, continuous daily administration of d-PEN was necessary for it to be effective. A single dose of d-PEN (1 m Mol/kg, ip) administered one hr after [14C]-DTB (1 mg/kg, ip) did not affect the plasma and tissue concentrations of DTB-derived radioactivity or their corresponding elimination kinetics. Cumulative urinary and fecal excretion of DTB-derived radioactivity were also unaffected by d-PEN administration as were the relative proportions of DTB and two of its metabolites, monothiobiuret and thiuret, in urine. Other agents that produced dose-dependent antagonism of DTB toxicity were diethyldithiocarbamate, disulfiram, cysteamine and 2,2'-dipyridyl. Considering the chemical and biological properties of DTB and its antagonists, a mechanism of antagonism involving an alteration of the thiol-disulfide and/or divalent metal cation status of motor axon terminals is postulated.

2,2'-Dipyridyl↗
PubMed1985

[Treatment of lead poisoning by drinking water using hemofiltration and chelationin a hemodialysed anuric patient].

Lead intoxication was diagnosed in April 1984 in an anuric woman of 65 years of age, whose hemodialysis had begun 9 years previously. Lead poisoning was completely cured by repeated hemofiltration with calcium EDTA. 28.2 mg of lead were extracted during 26 hemofiltration sessions. After the twentieth session, the rate of extracted lead was 500 micrograms per session and the rate of delta-aminolevulinic acid dehydrase was normalized. This exceptional observation allowed a nearly experimental study of the kinetics and metabolism of Ca EDTA chelated lead.

Aged↗
PubMed1989

Hypernatremia.

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.

Animals↗
PubMed1991

Reversible Schwann cell hypertrophy in lead neuropathy.

Schwann cell hypertrophy is an early change observed in lead-induced neuropathy in the rat. In order to quantify this cell hypertrophy, a morphometric analysis of Schwann cell cytoplasmic and nuclear areas and their relationship to the cross-sectional area of the associated myelinated fibre was performed. The study was carried out on sural and peroneal nerves from three groups of adult rats. Group I was intoxicated with 4% lead acetate in the drinking water for 6 weeks; group II animals were treated as in group I and then restored to standard laboratory conditions for 30 days; and group III were controls. The results showed that: (a) after 6 weeks of lead exposure, cytoplasmic and nuclear areas were significantly greater in intoxicated, compared with control rats; (b) after 30 days recovery, Schwann cell cytoplasmic and nuclear areas did not differ from control rats.

Animals↗
PubMedDate not supplied

[Effect of transurethral resection of the prostate on the state of patients with ischemic heart disease].

The water-salt equilibrium and the degree of endogenous intoxication (albumin fluorescence test) were examined in 60 patients with transurethral resection of the prostate (TURP), 40 of whom had ischemic heart disease (IHD). Body temperature, ECG, ST segment and echocardioscopy were daily monitored perioperatively in all patients. The results showed a lack of any pronounced changes in the water-salt equilibrium in TURP that lasted up to 1.5 hours and included big volumes of 5% glucose; they were also indicative of a lower postoperative binding albumin ability, which is normally most pronounced in patients with hyperthermia. As for the IHD patients, hyperthermia was found to be concurrent in them with the onset of ischemia of the myocardium and with its low contractive ability, which can be referred to as a significant factor in case of the above patients.

Adenosine Triphosphate↗
PubMed1992

Effects of chronic ethanol administration on free radical defence in rat myocardium.

Cellular protection against free radical reactions was measured in myocardium from ethanol-fed rats using ethanol administration in drinking water as a model of moderate alcohol intoxication. The activities of Cu,Zn-superoxide dismutase (SOD) and glutathione-S-transferase were higher in ethanol-fed rats than in controls, whereas Mn-SOD, catalase and glutathione peroxidase activities were not altered by ethanol treatment. Myocardial zinc was higher and selenium concentration lower in ethanol-fed rats than in controls. Ethanol consumption, which failed to modify the myocardial vitamin E level, did not result in increased lipid peroxidation, but decreased cytosolic and membraneous protein thiols.

Alcohol Drinking↗
PubMed1994

Mitochondrial respiratory activity and superoxide radical generation in the liver, brain and heart after chronic ethanol intake.

Functional characteristics of mitochondria isolated from liver, brain and heart were studied in ethanol-fed rats using ethanol administration in drinking water as a model of moderate alcohol intoxication. Our results show a slight decrease in liver cytochrome aa3 content, the mitochondrial alteration which is most consistently observed during chronic ethanol feeding. In liver and heart mitochondria, ethanol consumption led to an increase in state 3 respiration with NAD(+)-linked substrates, whereas no changes were apparent in respiration rates with succinate as substrate. However a decrease was found in state 3 respiration with succinate in brain mitochondria isolated from ethanol-fed rats. Submitochondrial particles (SMP) were used to study the superoxide radical (O2-.) production at the level of antimycin-inhibited regions of the respiratory chain. It appears that there is no clear correlation between ethanol effects on respiration and O2-. production. Whereas O2-. generation remained unchanged in heart mitochondria, an elevation of O2-. generation was observed in brain mitochondria, and in contrast, the rate of O2-. production was decreased in liver mitochondria of the ethanol-group in comparison to the control-group. Our findings support a tissue specificity for the toxic effects of ethanol towards the mitochondria and indicate that mitochondrial free radical mechanisms are involved in ethanol-induced toxicity in the brain.

Alcohol Drinking↗
PubMed1979

The effect of external stimulus change on ethanol-produced dissociation.

Rats which were subjected to aversive Pavlovian conditioning while in a state of ethanol-produced intoxication showed significantly less conditioned suppression of water drinking in the non-drugged state only if the external stimulus situation was also changed between conditioning and testing. This interaction between internal and external stimulus change supports a generalization-decrement explanation of drug-produced dissociation of memory. The number of conditioning trials was also manipulated, but this variable had no significant effect on the conditioned responses. In a second experiment, ethanol injections were given again shortly before testing. This treatment caused a normal degree of conditioned drinking suppression in rats conditioned in the ethanol state, indicating that state-dependent learning was responsible for the conditioned response deficit seen in the first experiment. The dissociation was asymmetrical since rats injected with ethanol before testing only showed a high degree of conditioned suppression.

Animals↗
PubMed1997

Changes in some pro- and antioxidants in rat cerebellum after chronic alcohol intake.

Some pro- and antioxidants were measured in the cerebellum from ethanol-fed rats using ethanol administration in drinking water as a model of moderate alcohol intoxication. After 4 weeks of ethanol intake, a 30% increase in the nonheme iron content in the cerebellum occurred in ethanol-fed rats as compared to control animals. The low-molecular-weight-chelated iron (LMWC-Fe) content as well as the percentage of total nonheme iron represented by LMWC-Fe were increased in the cerebellar cytosol after chronic ethanol administration. Cerebellar copper and selenium concentrations were lower and zinc concentration higher in ethanol-fed rats than in controls. Ethanol consumption decreased the cerebellar vitamin E level. Glutathione S-transferase [EC 2. 5. 1. 18] activity was higher, whereas glutathione peroxidase [glutathione: H2O2 oxidoreductase, EC 1. 11. 1. 9] activity was not altered by ethanol treatment. No significant changes in cerebellar lipid peroxidation, carbonyl protein content, or glutamine synthetase [L-glutamate:ammonia ligase (ADP-forming) EC 6. 3. 1. 2] activity were observed. These results suggest that adaptative increases in some elements of the antioxidant defense may counteract the increase in LMWC-Fe, a pro-oxidant factor, and prevent the occurrence of overt cellular lipid and protein damage. However, after 8 weeks of ethanol intake, the activity of glutamine synthetase, an enzyme specially sensitive to inactivation by oxygen radicals, was decreased, suggesting that this prevention was not totally achieved.

Animals↗