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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of daily oral administration to young rats of lead (10 mg/kg) and ethanol (10%, v/v, in drinking water), either alone or in combination, for 8 weeks on the uptake of lead in tissues, brain biogenic amines, hepatic alcohol dehydrogenase and cytosolic and mitochondrial aldehyde dehydrogenase and some selected lead-sensitive variables. Lead given in combination with ethanol produced more pronounced inhibition in the activities of hepatic glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) as compared to lead alone treatment. Simultaneous exposure to lead and ethanol produced a greater depression of dopamine (DA) and 5-hydroxytryptamine (5-HT) levels in the whole brain of rats, compared to rats treated with lead alone. The concentrations of lead in blood, liver and brain were significantly higher in rats exposed simultaneously to lead and ethanol. Though ethanol treatment alone inhibited the activities of hepatic alcohol dehydrogenase and cytosolic and mitochondrial aldehyde dehydrogenase, no effect of lead treatment alone on these variables was observed. The results suggested that animals exposed to ethanol and lead are more vulnerable to the neurologic and hepatotoxic effects and the systemic toxicity of lead.
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PMID:Effect of combined exposure to lead and ethanol on some biochemical indices in the rat. 382 40

Certain developmental abnormalities have been associated with environmental exposure to lead and our previous studies have indicated that the endogenous opioid system is disrupted by this metal. In connection with this we report the ontogeny of proenkephalin products in the rat striatum determined by combined HPLC and bioassay and the effects of low-level lead exposure on this ontogeny. The development of Met-enkephalin levels was dissimilar from that of the other proenkephalin products, Met-enkephalyl-Arg6-Phe7, Met-enkephalyl-Arg6-Gly7-Leu8 and Leu-enkephalin. The ratios of Met-enkephalin containing peptides to Leu-enkephalin was less than the 6:1 ratio predicted from the proenkephalin structure. Lead (administered in the maternal drinking water, from conception to weaning at 100, 300 and 1000 ppm) caused a dose-related depression of the levels of proenkephalin products in rat striatum at 10, 21 and 30 days after birth. The most pronounced effects were observed at 10 days and the most persistent effects were seen with Met-enkephalin. Peak blood lead levels were below 45 micrograms/100 ml in the 100 and 300 ppm lead-dosed groups and in all lead-dosed groups at 10 days after birth. It is suggested that lead may have inhibitory effects on proenkephalin-processing enzymes.
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PMID:Ontogenesis of proenkephalin products in rat striatum and the inhibitory effects of low-level lead exposure. 404 20

The effects of post-natal exposure to lead on the development of the electroretinogram in rats were studied. Newborn rats were fed with lead acetate by gastric intubation and weight and age-matched control rats were given sodium acetate in a similar way. At 15 and 26 days of age the lead concentrations in blood were on average 298 micrograms/100 ml and 80 micrograms/100 ml, respectively. The brain concentrations of lead were on average 248 micrograms/100 mg in the 15-day-old lead-fed animals and 244 micrograms/100 mg in the 26-day-old ones. Lead produced a transient depression of the post-natal development of the electroretinogram. A decrease in the amplitudes of the a- and b-waves, as well as an increase in the peak times of these potentials were found in the 15-day-old animals. The ERGs of the 26-day-old animals did not differ from controls. There were no morphological changes of the retina.
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PMID:Studies on developmental alterations in the electroretinogram in rats after post-natal exposure to lead. 407 38

Effects of bath-applied lead acetate on nerve-evoked and spontaneous neurotransmitter release were studied at the neuromuscular junction of the rat using conventional microelectrode recording techniques. Lead (20, 100 microM) depressed end-plate potential (EPP) amplitude within 5 min of application without affecting miniature end-plate potential (MEPP) amplitude. Increasing bath Ca2+ concentration from 2 mM to 4 or 8 mM caused a concentration-dependent reversal of lead-induced block of nerve-evoked EPPs. When lead was washed out of the bath, EPP amplitude either returned to control values, or was potentiated. Mean quantal content (m) was reduced significantly by lead treatment, an effect due primarily to a decrease in the immediately available store of transmitter (n). The probability of transmitter release (p) was either unchanged or slightly increased by lead. In contrast to its depressant effect on evoked transmitter release, spontaneous transmitter release, as measured by MEPP frequency, was increased by lead. MEPP frequency was increased from control levels of 1.2-3.2/sec to 12-16/sec by 100 microM lead. When lead was removed from the bath solution, MEPP frequency returned to control levels. Lead-induced increases in MEPP frequency still occurred when Ca2+ was removed from the external bath solution, or when 1 mM Mn2+ was added to block nerve terminal Ca2+ channels, suggesting that extracellular Ca2+ is not required for lead to increase spontaneous release. It is suggested that lead exerts actions at multiple sites at the presynaptic nerve terminal. An extracellular action of lead on transmitter release mechanisms is likely to be due to a competitive antagonism with Ca2+ for entry through Ca2+ channels. An intracellular action of lead is indicated by the depression of n, and the ability of lead to stimulate spontaneous acetylcholine release in the absence of external Ca2+ entry.
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PMID:Mechanism of action of lead on neuromuscular junctions. 609 47

The effects of micromolar (1.0-60.0 microM) amounts of lead and of cadmium on the light response of photoreceptors were studied using the isolated, perfused bullfrog retina. The effect of lead in depressing rod activity is readily and fully reversible. Lead is very effective in depressing the rod response at concentrations as low as 1.0 microM, but the effect of lead saturates at about 25.0 microM with about 34% depression of the rod response. At the higher concentrations some spontaneous recovery of rod response amplitude is observed shortly after exposure of the retina to lead begins. The cone response is affected by lead only rarely and then only at the higher concentrations. When affected, the cone response is enhanced rather than depressed. The effects of cadmium are generally similar to those of lead. However, saturating concentrations of cadmium depress the rod response to a greater degree than lead and the cadmium effects are not as readily reversible as the effects of lead at the higher concentrations. Cones are much more sensitive to cadmium than they are to lead and 60.0 microM cadmium always enhances cone response amplitude. The results of experiments in which lead and cadmium were both added to the retinal perfusate indicate to us that cadmium and lead both affect the same sensitive site or sites responsible for generating the rod response, but that cadmium affects an additional site that is not sensitive to lead. The depressive effects of lead and of cadmium on the rod response are discussed in terms of the postulated mechanisms of transduction in the vertebrate photoreceptor.
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PMID:The effects of lead and of cadmium on the mass photoreceptor potential: the dose-response relationship. 630 84

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.
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PMID:Practical toxicologic diagnosis. 649 3

The effects of nickel chloride were studied in two human cell lines, HeLa and diploid embryonic fibroblasts, as well as in V79 Chinese hamster cells and in L-A mouse fibroblasts. NiCl2 produces a dose-dependent depression of proliferation and mitotic rate. Effects on viability are accompanied by an increasing release of the intracellular enzyme lactic dehydrogenase. Lactic acid production is stimulated. The plating efficiency is reduced, as are DNA and protein synthesis and, to a lesser degree, RNA synthesis. Comparing these results with those of previous studies of the cytotoxicity of other heavy metals in the same test systems, similar effects are observed though with different intensities and slight differences between the cell lines employed. As regards lethal effects (LC50) the following rank order of cytotoxicity can be established: Ni2+ approximately equal to Pb2+ less than Mn2+ less than Hg2+ less than Cd2+; as regards growth inhibition the same rank order is observed as in the case of the LC50 in HeLa and human fibroblasts, but in L-A cells Ni2+ is more inhibitive than the other metal ions listed above with the exception of Cd2+. With respect to colony formation NiCl2 is less effective than PbCl2, MnCl2, and CdCl2. NiCl2 effects in serum-free medium are much faster and more severe than in medium containing serum or serum albumin indicating that serum constituents, notably albumin, bind the metal effectively and inhibit cellular uptake; this confirms reports of other authors on the serum binding and slow uptake of NiCl2. Synchronized cells are most sensitive in the G1 and early S phases of the cell cycle. Together with the finding that thymidine incorporation is affected to a considerable degree this contributes an explanation of the known genotoxic effects of nickel.
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PMID:Toxicity of nickel for mammalian cells in culture. 672 Jan 41

Ten clinically normal male beagle dogs were used in the study. Two dogs served as control, 4 received 2 mg lead/kg daily and 4 received 5 mg lead/kg/daily. Lead was administered for 13 weeks, after which one-half of each experimental group was treated with calcium ethylene diaminetetraacetate (CaEDTA) for 5 days. All animals were then monitored for another 4 weeks. Blood lead levels, haematology, blood glutathione concentration, and the number of bone marrow cells with stainable iron granules were measured weekly during the 18-week experimental period. Clinical signs of poisoning were observed only in one dog in the high dose group after 6 weeks. The signed included emaciation, anorexia, muscular weakness, evidence of abdominal pain and depression. These signs were reversed with cessation of lead dosing and CaEDTA treatment. Blood lead levels and the number of marrow cells with non-haeme iron increased in both lead-dosed groups; nucleated red blood cells increased only in high lead dosed group. There was a trend for an increased packed cell volume in all groups; however, the high lead dosed group did not increase as fast. No significant changes were observed in blood glutathione concentration and in other haematologic parameters. There were no differences in the parameters studied between the dogs treated with CaEDTA and those not so treated. Blood lead levels and the number of nucleated red blood cells decreased after cessation of lead administration and the number of marrow cells with iron also tended to decrease after lead removal.
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PMID:Effect of chronic lead on the haematology, blood glutathione and bone marrow non-haeme iron of dogs. 676 21

The effect of chronic oral led acetate administration on canine bone marrow was studied. Two dogs (group 1) were used as controls, 4 dogs (group 2) were given 2 mg of lead/kg of body weight daily, and 4 dogs (group 3) were given 5 mg of lead/kg daily. After a 7-day stabilizaion period, lead dosing was conducted for 91 days (13 weeks), after which half of each group was treated with calcium ethylenediaminetetraacetic acid. All dogs were then observed for another 28 days (4 weeks). Blood lead values and bone marrow cellular changes were monitored once a week during the 126 days (18 weeks) of study. Lead-dosed dogs had lower weight gains than the controls. Clinical signs of toxicosis were observed after 6 weeks in one dog in group 3. Anorexia, body weight loss, CNS depression, muscular weakness, and trembling were seen. Blood lead concentrations increased in all group 2 and 3 dogs. Lead caused increases in bone marrow segmented neutrophils and myeloid series cells, and increased myeloid:erythroid ratios. Blood lead concentrations and myeloid:erythroid ratios decreased after cessation of lead administration.
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PMID:Effect of chronic lead exposure on the canine bone marrow. 677 50

Diets containing 150 or 600 ppm magnesium with or without 200 ppm lead were fed to rats throughout gestation and lactation to determine the influence of moderate magnesium deficiency on tissue lead content of maternal and offspring tissue. During lactation it was necessary to increase the lowest dietary magnesium level to 225 ppm. Lead caused a significant depression in both gestational weight gain and average pup weight regardless of the level of dietary magnesium. Maternal magnesium deficiency was evidenced by significant reductions in serum and tibia magnesium, a 17-fold increase in kidney calcium, and hyperemia of the ears. In offspring, however, only growth and tibia magnesium were significantly affected by the magnesium deficiency, and the maternal-fetal difference in serum and tibia magnesium concentration was maintained. Maternal magnesium deficiency resulted in significantly higher lead concentrations in dam liver, and offspring erythrocytes, liver and tibia. A mechanism for the enhanced accumulation of lead in maternal and offspring tissue as a result of maternal magnesium deficiency is not defined, but it is likely to involve enhanced intestinal lead absorption.
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PMID:Influence of maternal magnesium deficiency on tissue lead content of rats. 686 42


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