Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of sublethal waterborne Zn2+ (150 micrograms l-1 = 2.3 mumol-1) on the kinetics of unidirectional Ca2+ influx were studied in juvenile freshwater rainbow trout during chronic exposure (60 days) at a water [Ca2+] of 1.0 mmol l-1. An unexposed group held under identical conditions served as control. The presence of Zn2+ in the water increased the apparent Km for Ca2+ influx by up to 300% with only a small inhibitory effect (35% at most) on the maximum rate of uptake (Jmax). These results, in combination with earlier data showing that Ca2+ competitively inhibits Zn2+ uptake, suggest that Zn2+ and Ca2+ compete for the same uptake sites. Acute withdrawal of Zn2+ after 3h of exposure resulted in a 23-fold reduction in Km for Ca2+, but a persistent small depression of Jmax. During prolonged exposure to Zn2+, the apparent Km for Ca2+ remained greatly elevated and Jmax remained slightly depressed. The actual Ca2+ influx in hard water ([Ca2+] = 1.0 mmol l-1) decreased marginally and paralleled the small changes in Jmax. The increases in apparent Km had a negligible influence on the actual Ca2+ influx because Km values (38-230 mumol l-1), even when elevated by Zn2+, remained below the water [Ca2+] (1000 mumol l-1). Rainbow trout exposed to Zn2+ exhibited a slower rate of protein synthesis in the gills (measured on day 23) and an increased tolerance to Zn2+ challenge (measured on both days 27 and 50). Unidirectional Zn2+ influx, measured at the end of the exposure period, was significantly reduced in the Zn2+-exposed fish. There were no changes in hepatic or branchial Zn2+, Cu2+ or metallothionein concentrations. We hypothesize that, during exposure to sublethal [Zn2+] in hard water, the fish may change the Km for a mutual Ca2+/Zn2+ carrier so as to reduce markedly Zn2+ influx without greatly altering Ca2+ influx. This reduced Zn2+ influx, rather than metallothionein induction, may be the basis of adaptation to elevated concentrations of waterborne Zn2+.
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PMID:Effects of zinc on the kinetics of branchial calcium uptake in freshwater rainbow trout during adaptation to waterborne zinc. 752 31

Desferrioxamine (DFO) is the most important drug in the treatment of thalassemia major and other hematological diseases requiring regular transfusion. It eliminates excessive ferritin by building up chelate complexes. Different mechanisms of possible DFO toxicity are induction of oxidation, damage of the blood-retina barrier, or reduction in other metalloions (Cu2+, Zn2+). The objective of the present study was to evaluate the ocular side effects of DFO treatment. We prospectively examined 17 patients aged 5 to 25 years, all of them treated with DFO. Visual acuity, pupillary reaction, anterior segment, lens and fundus were checked. If possible, visual fields, color vision, dark adaptation, stereoscopic vision, and contrast sensitivity were investigated. Lens opacities were found in 41% (7/17), changes in the retinal pigment epithelium in 35% (6/17), tortuosity of retinal vessels in 24% (4/17), dilation and sheathing of the retinal vessels in 18% (3/17), defects in color vision in 29% (5/17), and abnormal dark adaptation in 18% (3/17) of the patients. The oculotoxicity of DFO is dose-dependent. Major side effects like depression of the visual acuity are partially reversible after discontinuing the therapy. Regular ophthalmological check-ups are therefore necessary.
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PMID:[Ocular findings in Desferal therapy]. 771 74

The appearance of joint inflammation (JI) 14 days after the injection of adjuvant (AJ) in the tail of rats is associated with a cachectic syndrome which is characterised by marked weight loss (WL). The degree of weight loss was examined in relation to the extent of change in other markers of inflammation including increased plasma copper (pCu), decreased plasma zinc (pZn) and increased hepatic metallothionein (hMT). At 14 days post-AJ injection, arthritic rats showed the following changes, relative to the controls: body weight, 12% decrease, pZn, 50% decrease; pCu, 90% increase and hMT, 11-fold increase (all p < 0.001). Significant relationships were observed between JI, WL, pZn and hMT. The following coefficients of determination (r2) were observed; JI and WL, -0.530, JI and pZn, -0.485; JI and hMT, 0.286; WL and hMT, -0.510 (all p < 0.007). There was a strong relationship between the decreased pZn and increased hMT; r2 = 0.456 (p < 0.001). While increased pCu was clearly associated with AJ-arthritis in these rats, there was no quantitative relationship between the extent of change in pCu and the other parameters measured (r2 all < 0.01). The highest correlation observed was between pZn and WL (r2 = 0.637, p < 0.001). While the initial depression of pZn may be the result of increased hepatic hMT levels, longer term reductions in pZn levels are linked to systemic inflammation, the degree of arthritis and associated weight loss.
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PMID:Wasting in adjuvant-induced arthritis and its relationship to plasma zinc, copper and liver metallothionein. 784 86

Two sexually intact female silver-shaded domestic ferret siblings from different litters were examined because of CNS depression and lethargy. Ferret 1 was dehydrated and hypothermic, whereas ferret 2 was icteric and febrile and had serum bilirubin concentration > 12.0 mg/dl and BUN of 59 mg/dl. Despite supportive treatment, the ferrets died within days of evaluation. On necropsy, ferret 1 had chronic hepatopathy, with diffuse vacuolation of hepatocytes. In ferret 2, the liver had centrilobular degeneration and necrosis, and hemoglobinuric nephrosis was evident, with hemoglobin in the renal tubules. In both ferrets, Kupffer's cells and macrophages contained eosinophilic material in the cytoplasm. Special staining revealed copper pigment in hepatocytes and phagocytic cells in both livers. Analysis of liver specimens revealed 850 and 700 ppm of copper in ferrets 1 and 2, respectively. Copper values > 200 ppm in liver are considered evidence of toxicosis in most animal species. Copper toxicosis was diagnosed on the basis of the findings from histologic examination of the liver and high hepatic copper values. Lack of related illness in 11 other ferrets in the same environment and fed the same diet, plus sibling relationship and same phenotypic coat color in the affected ferrets, suggested that these ferrets had an inherited defect in their ability to metabolize normal amounts of ingested copper.
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PMID:Copper toxicosis in sibling ferrets. 789 May 74

To investigate the changes in salivary secretion associated with emesis, salivary secretion from the submaxillary gland and centrifugal discharge from the parasympathetic postganglionic nerve fibers from the submandibular ganglion were measured after emetic stimulation in chloralose-anesthetized and paralyzed dogs. In the basal condition, saliva flow and the basal frequencies of single unit discharges from the parasympathetic nerve were very low. Esophageal and gastric distension and lingual nerve afferent stimulation generally increased salivary secretion and nerve activity. Administration of apomorphine (0.2-0.3 mg/kg im) or intragastric infusion of copper sulfate (10%, 50 ml) elicited an excitation of parasympathetic nerve activity, and salivary secretion was facilitated in parallel to this nerve activity. The excitatory responses induced by emetic stimulation were suddenly depressed in correspondence with retching activities. This depression in nerve activity appeared 200-400 ms after the beginning of retching volleys of the phrenic nerve and continued during retching. These results indicate that the salivary center receives excitatory and inhibitory inputs from two different sources before and during retching activities, respectively.
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PMID:Canine salivary secretion from the submaxillary glands before and during retching. 797 43

Broiler chicks were kept on feeds amended by the addition of 240 mg monensin and 15 mg selenium with or without 200 mg vitamin E/kg. After 12 days, birds in different groups were orally administered three doses of 250 mg monensin and 5 mg selenium/kg body weight. In the second experiment, after four weeks of adaptation on amended feeds, similar groups were orally administered 40 mg monensin and 1 mg selenium/kg body weight on alternate days for four weeks. Monensin increased the liver iron level. Selenium increased the hepatic levels of selenium and iron while variable degrees of depression occurred in copper, zinc, manganese and magnesium levels. Concurrent administration of monensin and selenium significantly increased the liver selenium levels. A marked decrease in body weight and increased mortality were recorded due to concurrent administration of monensin and selenium.
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PMID:Concurrent oral administration of monensin and selenium to broiler chickens: effects on concentration of different elements in the liver. 801 40

The interactions between different heavy metal compounds which affect their cytotoxicity towards rabbit alveolar macrophages were investigated. The cells were exposed in vitro to combinations of As3+, Cd2+, Hg2+, Ni2+, or V5+ with different concentrations of another heavy metal compound. Toxicity was determined as the depression of zymosan-induced release of superoxide anion radicals. Significant antagonisms occurred in the combinations Cd2+/Zn2+, Hg2+/As3+, and Hg2+/Se4+, while significant synergisms were exhibited by the combinations Cd2+/Cu2+, Cd2+/Sn2+, Hg2+/Cu2+, Ni2+/Cd2+, Ni2+/Cu2+, Ni2+/Sn2+ and V5+/Cu2+. In the combinations As3+/Zn2+, Hg2+/Cd2+ and Hg2+/Zn2+, both kinds of interactions were observed depending on the concentrations of the heavy metal compounds. An interpretation of the measured heavy metal interactions with reference to the toxicity of heavy metal-containing dusts is attempted.
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PMID:Cytotoxicity of dust constituents towards alveolar macrophages: interactions of heavy metal compounds. 813 19

Broiler chicks fed lead or selenium for varying periods were later intoxicated with two levels of either of these elements. In this way different groups of chicks were exposed to lead or selenium alone or a combination of these two. Lead caused increased liver concentrations of lead and iron. Selenium administration increased liver selenium and iron levels while liver copper decreased. Concurrent administration of lead and selenium greatly enhanced the accumulation of both elements in the liver and increased the liver iron. Lead partially counteracted the depression of liver copper caused by selenium. Mortality due to concurrent exposure to lead and selenium was lower when vitamin E was added to the feed. Body weights were markedly suppressed by selenium. The concurrent administration of lead partially alleviated the growth depression caused by selenium. Selenium fed birds had increased relative weights of liver and heart but this increase was of lesser degree in birds given both elements.
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PMID:Effects of oral administration of toxic levels of lead and selenium upon concentration of different elements in the liver of broiler chicks. 813 71

Dietary copper deficiency impairs cardiovascular function by depression of catecholamine metabolism, and alteration of the structure and function of cardiac mitochondria. Heat shock proteins (HSPs) are a group of cellular homeostatic proteins that are induced in vascular tissue by catecholaminergic transmission after exposure to stress. We investigated the effects of dietary copper deficiency on the induction and accumulation of HSPs in several cardiovascular tissues. Stress-induced levels of aortic HSP70 mRNA were reduced in copper-deficient (CuD) rats when compared with copper-adequate (CuA) controls. Cocaine-induced HSP70 mRNA accumulation was not different between CuA and CuD rats, suggesting that reduced HSP70 levels in restrained CuD animals may result from altered catecholaminergic neurotransmission. The level of HSP60 mRNA was specifically reduced in the atria of CuD rats, which may be associated with altered mitochondrial structure and function. These results describe a novel relationship between dietary copper deficiency and the expression of highly conserved cellular stress response proteins. Loss of these essential homeostatic proteins in vascular tissue may contribute to the impairment of cardiovascular function known to accompany copper deficiency.
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PMID:Dietary copper deficiency reduces heat shock protein expression in cardiovascular tissues. 829 95

Rats (Wistar, female, 4 weeks old) were fed iron-deficient (Fe-; 2.2 micrograms Fe/g) or manganese- and copper-deficient (Mn.Cu-; 0.3 microgram Mn/g, 0.4 microgram Cu/g) diets for 8 weeks to determine the oxidative damage of DNA by element deficiency. After feeding of the diets, 2-nitropropane (2-NP, 80 mg/kg body weight) was administered i.p. as an inducer of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) to the element-deficient rats. The hemoglobin concentration of rats in the Fe- group showed an induction of severe anemia (8.4 g/100 ml whole blood). In the Mn.Cu- group, Mn-superoxide dismutase (SOD) activities of plasma and Cu.Zn-SOD activities were significantly lower than that of the normal diet group. However, total SOD activities of plasma were not depressed severely in contrast to that of the liver in the Mn.Cu- group. Background (spontaneous) levels of 8-OH-dG in normal diet group were 0.96 +/- 0.37/10(5) deoxyguanosine (dG), however, significantly higher levels were detected in the Fe- group (1.56 +/- 0.19, P < 0.01). Conversely, a lower (but not significant) level of 8-OH-dG than the normal diet group were detected in the Mn.Cu- group (0.78 +/- 0.08). Six hours after 2-NP treatment, 8-OH-dG levels in liver DNA were significantly induced to 1.44 +/- 0.24 in the normal diet fed group 1.89 +/- 0.22 in the Fe- and 1.08 +/- 0.12 in the Mn.Cu- groups. Compared to the normal diet group, these induced levels of 8-OH-dG in the Fe- group were significantly higher (P < 0.05), and that in Mn.Cu- group were significantly lower (P < 0.05). The high level of 8-OH-dG in severe iron deficiency might be the results of: (i) an increase of hydroxyl radical generation by accumulated copper in hepatocytes; or (ii), a depression of enzymatic activity for removing 8-hydroxy-2'-deoxyguanosine in DNA, which is dependent on divalent cations. On the other hand, the low level of 8-OH-dG in manganese and copper deficiency might be the result of a decrease of lipid peroxidation which has been suggested to be an intermediator from active oxygen species to hydroxyl radical.
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PMID:Spontaneous and 2-nitropropane induced levels of 8-hydroxy-2'-deoxyguanosine in liver DNA of rats fed iron-deficient or manganese- and copper-deficient diets. 838 15


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