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)

Cattle had severe signs of toxicosis when gavaged dried ground Thermopsis montana (false lupine, poison bean, mountain thermopsis) at doses of 0.6-2.8 g/kg/day in a water suspension. Signs included depression, anorexia, swollen eye lids, arched back, tucked abdomen, rough hair coat, and in extremis a prolonged recumbency lasting up to 9 days. Plant potency varied among collections. Total alkaloid doses in collections eliciting severe signs varied from 1.1-11.3 mg/kg/day. There were 5 major alkaloids in each collection that varied in concentration among the collections perhaps accounting for variation in severity of signs elicited. Four of the alkaloids were identified by GC retention time, MS fragmentation patterns and OR analysis as N-methylcytisine, cytisine, (-)-thermopsine, and (-)-anagyrine. Measurements showed a very marked increase of 10X-20X in levels of certain serum enzymes--SGOT, CPK, and LDH that persisted during the period of maximum clinical signs.
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PMID:Toxicity of Thermopsis montana in cattle. 369 96

The study of patterns of serum AST, ALT, CPK, LDH, and glycogen phosphorylase (GP) activity following bicycle ergometry in 26 male patients 1 to 1.5 months after myocardial infarction demonstrated no increase in AST, ALT and CPK activity, whereas total LDH activity was increased, with a tendency to elevated LDH-1 and LDH-2 fractions, as compared to the baseline, in those cases where exercise was discontinued because of ST depression. Patients with favorable response to bicycle ergometry that continued until the submaximum heart rate for a given age was achieved showed a tendency to elevated LDH-5 that may be a physiological response to exercise. The demonstrated increase in total GP activity, both in patients with exercise-induced ST depression and in those with elevated ST from the leads corresponding to the site of myocardial infarction, may reflect stress-induced reversible ischemia.
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PMID:[Effect of physical loading on serum enzyme activity in post-myocardial infarct patients]. 370 99

The lethal and non-lethal effects of L-buthionine-SR-Sulfoximine (BSO) with the sulfhydryl-dependent anticancer agents (SHDAA) were investigated in mice. The agents studied included carmustine (BCNU), cyclophosphamide (CTX), doxorubicin (DOX) and melphalan (LPAM). It was shown in normal mice that BSO is nontoxic when given IP or PO at a dose 5 g/kg. In pharmacodynamic studies with two different doses of BSO in CD-1 mice, the liver, kidney and heart demonstrated diurnal variations in thiol content and dose-dependent depression of tissue non-protein sulfhydryl (NPSH) levels. In acute lethal survival studies, mice treated with CTX and BSO exhibited increased lethality with seizures as a possible cause of death. This effect was not seen with BCNU, DOX and LPAM. Evaluations of organ-specific biochemical markers, showed slight elevations in LDH enzyme levels while bone marrow suppression was not enhanced using both in vivo spleen colony assay and in vitro colony forming unit myelotoxicity assays. These results show that the addition of BSO with SHDAA enhances the acute lethality of some agents such as CTX, and may also increase the non-myelosuppressive toxicities of other agents. It is recommended that BSO be used with caution in combination with SHDAA and that monitoring of hepatic enzymes be routinely performed.
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PMID:Lack of enhanced myelotoxicity with buthionine sulfoximine and sulfhydryl-dependent anticancer agents in mice. 382 7

The effects of antiarrhythmic drugs, aprindine, mexiletine and lidocaine, on rat erythrocytes, isolated rat hepatocytes and DPPC-liposomes were studied at various concentrations. Maximal inhibition of aprindine on the hypotonic hemolysis was observed at a concentration of 2 X 10(-4) M. In isolated rat hepatocytes, aprindine caused an increase in GOT leakage above 4 X 10(-4) M. Mexiletine and lidocaine caused a slight decrease in GOT. Only aprindine caused an increase in LDH leakage above 2 X 10(-4) M. In the relationship between the surface tension and pH conditions (pH 5.7, 7.4 and 8.0), aprindine and mexiletine indicated a depression of surface tension at a dose of 10(-4) M to 10(-3) M under all pH conditions. Lidocaine indicated a depression of surface tension at a dose of 10(-4) M at pH 8.0 only. Aprindine and mexiletine depressed the phase transition temperature (Tc) of DPPC-liposomes. The depression of Tc by aprindine was greater than that by mexiletine. The rank by order of surface activity was the same as that of enzyme leakage from hepatocytes, hemolysis of erythrocytes and depression of Tc in DPPC-liposomes in vitro. These results suggest that differences in membrane damage produced by antiarrhythmic drugs may by related to surface activity, which in turn may determine the extent of adsorption onto cell membranes.
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PMID:[Effects of antiarrhythmic drugs on rat erythrocytes, isolated hepatocytes and dipalmitoyl phosphatidyl choline (DPPC)-liposomes]. 384 Jan 13

Implantation of cobalt-agar rods into the visual cortex of 16 adult rats induced in some of the animals epileptiform bioelectrical activity and provoked in all of them histological and histochemical changes in the region of the implantation (primary focus) as well as in some ipsilateral projection sites of the visual cortex (secondary foci). The changes within the secondary foci are demonstrated in the Corpus geniculatum laterale, pars dorsale (dLGN), by means of 18 histochemical and 5 histological methods. Together with the appearance of hyperactive and degenerating neurones combined with neuronophagy and diminution of the number of synapses a marked gliosis developed, especially an increase of microglia. The destruction of the tissue induced a depression of energy and transmitter metabolism and intensified lytic processes. This is confirmed by the decreased activities of LDH, SDH, GPDH, G6PDH, NAD(P)H-TR, GABA-T and GDH and the increased activity of acid phosphatase in the neuropil of the secondary foci. Single hyperactive nerve and glial cells were accented by high activities of those enzymes which had a reduced activity in the neuropil. Since in our experiments agar-rods without cobalt never induced histological or histochemical changes in subcortical grisea of the visual system, the secondary foci seem to result from the direct influence of the cobalt, migrating in the corticothalamic projection pathway and identifiable in the dLGN by the TIMM technique.
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PMID:[Morphologic and histochemical changes in the secondary focus following cobalt-induced epileptogenic bioelectrical activity of the visual cortex in the adult rat]. 393 55

Biochemical parameters in 20 sheep were investigated following administration of quinuronium sulfate or diminazene diaceturate. The usual signs of salivation, micturition, anorexia, depression, muscular tremors and ataxia were observed within 20 min in sheep receiving therapeutic and double doses of quinuronium sulfate. There was an increased dose dependent plasma LDH activity above baseline values following administration of quinuronium sulfate and a non-dose dependent increased trend in diminazene diaceturate treatment. Plasma CK activity had an increased trend (p less than 0.05) above baseline values following administration of the two babesicides. Plasma BUN levels increased significantly (p less than 0.05) following administration of the two drugs. This study indicated that quinuronium sulfate is more organotoxic and hypotensive than diminazene diaceturate at therapeutic and/or above therapeutic dosages.
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PMID:Comparative studies of the effects of quinuronium sulfate and diminazene diaceturate in sheep. 408 73

The effects of N-nitrosothiazolidine (NNT) and N-nitrosomorpholine (NNM) on different biological parameters were investigated and compared. The oral LD50 value of NNT (1950 +/- 85 mg/kg) showed that it was about 6 times less toxic than NNM (LD50 = 320 mg/kg, po; Druckrey et al., 1967). Lethal and near-lethal doses (greater than or equal to 1500 mg/kg, po) of NNT caused central nervous system depression (reduced spontaneous motor activity, loss of righting and pain reflexes, without loss of consciousness), stereotypical behavior such as, purposeless chewing jaw movements lasting more than one hour, muscular rigidity, and in some rats, rare and brief clonic convulsions, 3 to 24 h after dosing. These neurotoxic signs, as a whole, were reminiscent of opioid intoxication. Rats that died after NNT-treatment had kidney necrosis in the distal tubules, but all survivors had normal kidneys. NNT (500 and 1000 mg/kg, sc) had no effect on the relative liver weights, but it inhibited liver mitosis at 24, 48, and 72 h after treatment. NNM (100 mg/kg, sc) decreased the relative liver weights on 3 posttreatment days; it inhibited liver mitosis after 24 h and enhanced it after 48 h in male rats. Both NNT and NNM increased the relative adrenal weights, but only NNM enhanced adrenocortical mitosis. In general, NNT had no effect on serum enzymes (SGOT, SGPT, LDH, HBDH), but it increased blood urea nitrogen (BUN) and serum creatinine 24 h after administration. Pretreatment of rats with 3 doses of NNT (150 mg/kg X d, po) increased the pentobarbital-induced sleep (PST) by 26% (not significant), while 3 doses of NNM (50 mg/kg X d, po) increased PST by 188%. In addition, NNM caused a severe centrilobular liver necrosis and glycogen depletion, associated with a marked rise in serum enzymes (SGOT, SGPT, LDH, HBDH) and fall in serum glucose. Compared with NNM, NNT, which was found in fried bacon (Kimoto et al., 1982; Gray et al., 1982), seemed to be a relatively nontoxic nitrosamine.
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PMID:Comparison of the acute toxicities of N-nitrosothiazolidine and N-nitrosomorpholine. 649 89

New antitumor anthracycline antibiotic, aclacinomycin A was given to dd-mice and Wistar rats for acute toxicity study. The LD50 values were 29 approximately 39 mg/kg (i.v., i.p. and s.c.) and 62 approximately 69 mg/kg (p.o.) in mice, and 18 approximately 28 mg/kg (i.v., i.p. and s.c.) and 58 approximately 59 mg/kg (p.o.) in rats, respectively, which were calculated by mortality rate during a 14 day observation period. Depression of spontaneous activity, anorexia, diarrhea and slight alopecia were observed. Autopsy findings in animals killed by drug included atrophy of the thymus and spleen, and hyperemia and hemorrhage in the stomach and intestines. But no remarkable change was found in animals which survived through the observation period. Mongrel dogs were given the drug intravenously at 3, 5, 7.5, 10 and 15 mg/kg, respectively. All dogs (3/3) in the three higher dose groups and 1/3 dog in 5 mg/kg dose group died within day 0 approximately 5. Others survived more than 27 days. Depression of spontaneous activity and anorexia were found from 30 minutes to 2 hours after administration, followed by vomiting and diarrhea. Increase of GOT, GPT and LDH and decrease of WBC count were detected in dogs which died. Hyperemia and hemorrhage of the lungs, stomach and intestine were found among the groups given higher doses, whereas no significant changes were recognized among the two lower dose groups.
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PMID:[Acute toxicity of aclacinomycin A in mice, rats and dogs (author's transl)]. 692 57

Seven patients with advanced cancer underwent whole-body hyperthermia using a nylon and vinyl mesh, water-perfused suit. Treatments were given at 41.8 degrees C for 4 hours. Five patients received concomitant cyclophosphamide with hyperthermia. Compared to baseline (37 degrees C) conditions, there was a significant rise in pulse rate (P less than 0.001), a fall in diastolic pressure (P less than 0.02), and an increase in respiratory rate (P less than 0.001). Toxic effects included fatigue, extremity edema, diarrhea, nausea and vomiting, and respiratory depression in a patient with cerebral metastases. Compared to baseline values, there was a significant increase in serum glucose (P less than 0.02) and decreases in serum calcium (P less than 0.01) and phosphorus (P less than 0.01). Significant elevations in serum LDH and SGOT values occurred 24 hours following hyperthermia, suggesting hepatic sensitivity to heat. The methods used to induce whole-body hyperthermia, as described in this paper, are feasible, permit relatively easy access to the patient, and are potentially applicable in diverse hospital settings such as intensive care units, radiation therapy areas, and conventional rooms. The physiologic alterations that were observed and the toxic effects that were documented indicate that careful monitoring of patients is necessary.
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PMID:Physiologic response and toxicity in patients undergoing whole-body hyperthermia for the treatment of cancer. 723 54

Magnesium--aluminum (Mg--Al) alloy wire was surgically implanted in the abdominal aorta and carotid and renal arteries of virgin (no arterial disease) and breeder (testicular and ovarian arterial lesions) spontaneously hypertensive rats (SHR). The Mg--Al implants promptly dissolved causing increased adrenal glandular weight, thymic involution, depression of the abnormally elevated blood pressure, and poor growth. Serum enzymes (CPK, SGOT, SGPT and LDH) were elevated, circulating levels of triglycerides and cholesterol were reduced, corticosterone and deoxycorticosterone secretion increased. Histologically, fibrocellular, intimal lesions, rich in ground substance, developed about the Mg-Al implants. Occlusive thromboses with cholesterol-positive clefts appeared in the Mg-Al-implanted carotid arteries of breeder SHR with preexisting arterial (limited to gonadal arterioles) disease. It is suggested that adrenocortical and gonadal hormonal factors may condition the responsiveness of the arterial wall of SHR to injury and repair.
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PMID:Pathophysiologic responses of spontaneously hypertensive rats to arterial magnesium--aluminum wire implants. 741 74


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