Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monkeys and rats were exposed to 11.6, 112.5, and 1152 micrograms Mn/m3 as an Mn3O4 aerosol twenty-four hours per day for nine months. Various evaluations of pulmonary function, electromyographic activity, limb tremor, and tissue manganese levels were conducted. No exposure related effects on pulmonary function, limb tremor, or electromyographic activity were observed. After nine months of exposure Mn levels were elevated in a near dose related manner in kidney, lung, spleen, and blood. However, by six months postexposure there were no differences as compared to the control group in tissue Mn levels which could be attributed to the exposure conditions.
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PMID:Evaluation of the chronic inhalation toxicity of a manganese oxide aerosol. III. Pulmonary function, electromyograms, limb tremor, and tissue manganese data. 11 36

The prevalence of neuropsychological and respiratory symptoms, lung ventilatory parameters, neurofunctional performances (visual reaction time, eye-hand coordination, hand steadiness, audioverbal short term memory), and several biological parameters (calcium, iron, luteinising hormone (LH), follicle stimulating hormone (FSH), and prolactin concentrations in serum, blood counts, manganese (Mn) concentration in blood and in urine) were examined in a group of workers (n = 92) exposed to MnO2 dust in a dry alkaline battery factory and a matched control group (n = 101). In the battery plant, the current exposure of the workers to airborne Mn was measured with personal samplers and amounted on average (geometric mean) to 215 and 948 micrograms Mn/m3 for respirable and total dust respectively. For each worker, the lifetime integrated exposure to respirable and total airborne Mn dust was also assessed. The geometric means of the Mn concentrations in blood (MnB) and in urine (MnU) were significantly higher in the Mn exposed group than in the control group (MnB 0.81 v 0.68 microgram/100 ml; MnU 0.84 v 0.09 microgram/g creatinine). On an individual basis, MnU and MnB were not related to various external exposure parameters (duration of exposure, current exposure, or lifetime integrated exposure to airborne Mn). On a group basis, a statistically significant association was found between MnU and current Mn concentrations in air. No appreciable difference between the exposed and the control workers was found with regard to the other biological measurements (calcium, LH, FSH, and prolactin in serum). Although the erythropoietic parameters and serum iron concentration were in the normal range for both groups, there was a statistically significant trend towards lower values in the Mn exposed workers. The prevalences of reported neuropsychological and respiratory symptoms, the lung function parameters, and the audioverbal short term memory scores did not differ between the control and exposed groups. The Mn workers, however, performed the other neurofunctional tests (visual reaction time, eye-hand coordination, hand steadiness) less satisfactorily than the control workers. For these tests, the prevalences of abnormal results were related to the lifetime integrated exposure to total and respirable Mn dust. On the basis of logistic regression analysis it may be inferred that an increased risk of peripheral tremor exists when the lifetime integrated exposure to Mn dust exceeds 3575 or 730 micrograms Mn/m3 x year for total and respirable dust respectively. The results clearly support a previous proposal by the authors to decrease the current time weighted average exposure to Mn dust.
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PMID:Assessment of the permissible exposure level to manganese in workers exposed to manganese dioxide dust. 173 53

Disturbances of movement and other motor functions can result from exposure to toxicants and drugs. Sometimes, as with acute exposure to ethanol or solvents, these effects disappear when exposure ends. Other times, as with manganese, haloperidol, or chronic ethanol, motor disturbances are irreversible and may even lie undetected until after exposure has ended. Motor disturbances can take on many guises, including tremor, difficulty in positioning, fatigue, or rigidity. Techniques for measuring these different endpoints in primates will be addressed. One preparation that enables the simultaneous monitoring of positioning, tremor, and operant behavior in nonhuman primates is described, and tactics for obtaining spectral estimates of tremor from a positioning task are outlined. The spectra obtained from this preparation are reliable and valid: they are stable over a period of a year, they correspond to spectra obtained from accelerometers, and are altered by acute administration of ethanol or oxotremorine. These two drugs had opposite effects on tremor but affected bar positioning in a similar manner.
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PMID:Quantification of motor function in toxicology. 314 Apr 29

Manganese (Mn) poisoning, a well-known hazard in miners and industrial workers, shares many features with Parkinson's disease. Two young agricultural workers with a parkinsonian syndrome, who mentioned exposure to the fungicide maneb (manganese ethylene-bis-dithiocarbamate), led us to investigate a new possible source of Mn intoxication. Fifty male rural workers with occupational exposure to maneb were compared with 19 rural workers without fungicide exposure. We noted significantly higher prevalence of plastic rigidity with cogwheel phenomenon, headache, fatigue, nervousness, memory complaints, and sleepiness in the exposed group. In addition, we saw other neurologic signs, such as postural tremor, cerebellar signs, and bradykinesia, although without statistical significance. The data suggest that occupational exposure to pesticides containing Mn is a possible source of Mn intoxication of the CNS.
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PMID:Chronic exposure to the fungicide maneb may produce symptoms and signs of CNS manganese intoxication. 335 9

Four monkeys were exposed to a total of 8 g each of manganese as oxide by repetitive subcutaneous injections during 5 months, after which they were left for 1 week to 6 months before they were sacrificed. All animals developed hyperactive behaviour after about 2 months. About 5 months after the start of the exposure the animals became hypoactive with an unsteady gait, and subsequently an action tremor appeared in some of the animals. The animals lost power in both upper and lower limbs and the movements of the hands and feet were very clumsy. The serum content of manganese rose 10-40 times during the exposure time and the content in brain was generally increased more than 10 times, with the highest content found in globus pallidus and putamen. The observed neurochemical effects were also largest in globus pallidus and putamen. In these regions there was a considerable depletion of dopamine and 3,4-dihydroxyphenylacetic acid, while the homovanillic acid content remained almost unchanged. A severe neuronal cell loss was observed in globus pallidus but not in other regions. This is in accordance with results from the most recent neuropathological study of a human suffering from chronic manganese poisoning [Yamada et al. (1986) Acta Neuropathol 70: 273-278] where globus pallidus was devoid of neuronal cells while the content of pigmented cells in substantia nigra was normal. Our data suggest a reduction in number of dopaminergic nerve terminals, as the activity of the dopamine synthesizing enzyme DOPA-decarboxylase was also lowered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of manganese oxide on monkeys as revealed by a combined neurochemical, histological and neurophysiological evaluation. 343 74

A cross-sectional epidemiological study was carried out among 141 male subjects exposed to inorganic manganese (Mn) in a Mn oxide and salt producing plant (mean age 34.3 years; duration of exposure, mean 7.1 years, range 1-19 years). The results were compared with those of a matched control group of 104 subjects. The intensity of Mn exposure was moderate as reflected by the airborne Mn levels and the concentrations of Mn in blood (Mn-B) and in urine (Mn-U). A significantly higher prevalence of cough in cold season, dyspnea during exercise, and recent episodes of acute bronchitis was found in the Mn group. Lung ventilatory parameters (forced vital capacity, FVC; forced expiratory volume in one second, FEV1; peak expiratory flow rate, PEFR) were only mildly altered in the Mn group (smokers) and the intensity and the prevalence of these changes were not related to Mn-B, Mn-U, or duration of exposure. There was no synergistic effect between Mn exposure and smoking on the spirometric parameters. Except for a few nonspecific symptoms (fatigue, tinnitus, trembling of fingers, increased irritability), the prevalence of the other subjective complaints did not differ significantly between the control and Mn groups. Psychomotor tests were more sensitive than the standardized neurological examination for the early detection of adverse effects of Mn on the central nervous system (CNS). Significant alterations were found in simple reaction time (visual), audioverbal short-term memory capacity, and hand tremor (eye-hand coordination, hand steadiness). A slight increase in the number of circulating neutrophils and in the values of several serum parameters (ie, calcium, ceruloplasmin, copper, and ferritin) was also found in the Mn group. There were no clear-cut dose-response relationships between Mn-U or duration of Mn exposure and the prevalence of abnormal CNS or biological findings. The prevalences of disturbances in hand tremor and that of increased levels of serum calcium were related to Mn-B. The response to the eye-hand coordination test suggests the existence of a Mn-B threshold at about 1 microgram Mn/100 ml of whole blood. This study demonstrates that a time-weighted average exposure to airborne Mn dust (total dust) of about 1 mg/m3 for less than 20 years may present preclinical signs of intoxication.
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PMID:Epidemiological survey among workers exposed to manganese: effects on lung, central nervous system, and some biological indices. 357 89

An autopsy case of a 52-year-old man suffering from chronic manganese poisoning (CMP) is reported with determination of the manganese distribution in the brain. The patient had been working in a manganese ore crushing plant since 1965. In 1967 he began to complain of difficulties in walking and diminished libido. Later, he developed various neuropsychiatric symptoms including euphoria, emotional incontinence, masked face, monotonous speech, "cock-walk", increased muscle tone, weakness of upper and lower extremities, tremor of the eye lids, and exaggeration of knee jerks. The major neuropathological change was degeneration of the basal ganglia, in which the pallidum was severely affected. The pallidum disclosed a loss and degeneration of nerve cells, which was especially marked in the medial segment, a prominent decrease of myelinated fibers, and moderate astrocytic proliferation. The substantia nigra was intact. Distribution of manganese in the brain of the present case of CMP was determined using flameless atomic absorption spectrometry and compared with control cases and also a case of Parkinson's disease (PD). There was no significant difference between the control cases and the case of PD in average concentration of manganese and its distribution in the brain. The present case of CMP showed no elevation in average concentration of manganese in the brain. However, there were some changes in its distribution. Thus, the continuance of neurological disorders in CMP is not linked to an elevated manganese concentration itself in the brain. CMP appears to be different from PD in neuropathology and manganese behavior in brain.
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PMID:Chronic manganese poisoning: a neuropathological study with determination of manganese distribution in the brain. 376 27

We have performed several cross-sectional epidemiological surveys among workers exposed to cadmium, mercury vapour or manganese in order to assess : their early biological or functional effects; the biological tests allowing an assessment of the amount of metal absorbed or stored in the body; the acceptable exposure levels. Studies have also been carried out among persons exposed to inorganic arsenic in order to define its inactivation mechanism and to develop a biological test of exposure. The kidney is the main critical organ following long-term exposure to cadmium. To prevent the occurrence of renal changes in the majority of male workers exposed to cadmium, its concentration in renal cortex should not exceed 215 micrograms/g (wet weight), and that in urine : 10 micrograms/g creatinine. A blood cadmium level of 1 microgram/100 ml has been suggested as maximum tolerable level for long-term exposure. Prolonged exposure to mercury vapour may lead to renal and neurological disturbances. The preclinical signs of nephrotoxicity are correlated with the amount of mercury absorbed which may be assessed by monitoring the mercury level in urine. The neurotoxic effects (particularly tremor) are mainly related to the integrated exposure (duration and intensity). A maximal permissible level of 50 micrograms Hg/g urinary creatinine is proposed to prevent the occurrence of these toxic effects. An exposure to manganese dust for 7 years on the average at a level below the maximum allowable airborne concentration (5 mg/m3) recommended by the ACGIH in the USA may still lead to a slight reduction in psychomotor and spirometric performances and interfere with calcium metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Biological aspects of occupational exposure to cadmium and several other metals]. 382 21

The interactions between the effects of manganese chloride and X-rays were studied in synchronized populations of V79 Chinese hamster fibroblasts. The cells were selected by shaking off asynchronous cultures for detachment of mitotic cells which were plated in petri dishes and exposed to various treatments. Irradiation was carried out with a Philips RT-100 X-ray unit. A final concentration of 0.25 mM MnCl2 was used. The main parameter was the colony forming ability of the surviving cell fraction. When MnCl2 was administered over 1 h, its toxicity was low regardless of the phase of the cell cycle. Administered separately, 2 Gy irradiation produced only a slight decrease in survival, less marked in the S phase. However, the two agents together induced a synergistic inhibition of the surviving fraction in the S phase when the metal was given immediately after irradiation. If manganese was administered 3 h after irradiation the two inhibitory effects apparently remained only additive. It seems that MnCl2 can impair some repair processes starting immediately after irradiation.
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PMID:Cell survival after the combined action of manganese (MnCl2) and X-rays in synchronized Chinese hamster cells. 651 8

The ionic requirements for electro-responsiveness in thalamic neurones were studied using in vitro slice preparations of the guinea-pig diencephalon. Analysis of the current-voltage relationship in these neurones revealed delayed and anomalous rectification. Substitution of Na+ with choline in the bath or addition of tetrodotoxin (TTX) abolished the fast spikes and the plateau potentials, described in the accompanying paper. Ca2+ conductance blockage with Co2+, Cd2+ or Mn2+, or replacement of Ca2+ by Mg2+ abolished the low-threshold spikes (l.t.s.). Substitution with Ba2+ did not significantly increase the duration of the l.t.s., suggesting that under normal conditions the falling phase of this response is brought about by inactivation of the Ca2+ conductance. The after-hyperpolarization (a.h.p.) following fast spikes was markedly reduced in amplitude and duration by bath application of Cd2+, Co2+ or Mn2+, indicating that a large component of this response is generated by a Ca2+-dependent K+ conductance (gK[Ca]). Following hyperpolarizing current pulses, the membrane potential showed a delayed return to base line. This delay is produced by a transient K+ conductance as it can be modified by changing the drive force for K+. Presumptive intra-dendritic recording demonstrated high-threshold Ca2+ spikes (h.t.s.s.) which activate a gK[Ca]. Such h.t.s.s. were also seen at the somatic level when K+ conductance was blocked with 4-aminopyridine. It is proposed that the intrinsic biophysical properties of thalamic neurones allow them to serve as relay systems and as single cell oscillators at two distinct frequencies, 9-10 and 5-6 Hz. These frequencies coincide with the alpha and theta rhythms of the e.e.g. and, in the latter case, with the frequency of Parkinson's tremor.
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PMID:Ionic basis for the electro-responsiveness and oscillatory properties of guinea-pig thalamic neurones in vitro. 673 93


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