Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Manganese Poisoning”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1995

Autoreceptor presynaptic control of dopamine release from striatum is lost at early stages of manganese poisoning.

Manganese (Mn) poisoning in man produces an early psychotic disorder that is later followed by a Parkinson-like syndrome. Since alterations in the brain DA system are thought to be involved, we assessed the presynaptic autoreceptor regulation of K(+)-evoked 3H-DA release from superfused striatal slices of mice treated i.p. with 5 mg Mn/kg weight/day for 2 and 8 weeks. Mn poisoning did not change basal and evoked DA release. In controls, 1 microM apomorphine (APO), a D2-like DA receptor agonist, produced an inhibition of K(+)-evoked 3H-DA release that was blocked by the D2-like DA receptor antagonist, S(-)-sulpiride (1 microM). Yet, APO lost its capacity to inhibit the K(+)-evoked 3H-DA release after 2 weeks of Mn poisoning. After 8 weeks of Mn poisoning, APO was again able to reduce K(+)-evoked 3H-DA release. MK-801 (0.3 microM), a NMDA-glutamate receptor antagonist, could restore APO inhibitory control on DA release lost at week 2 of Mn poisoning. These findings suggest a NMDA-glutamate-receptor-mediated loss of autoreceptor presynaptic control of striatal DA release at early Mn poisoning.

Animals↗
PubMed1984

Neurotransmitters and neurotransmitter receptors in developing and adult rats during manganese poisoning.

Manganese neurotoxicity has been recognized among industrial workers as a consequence of chronic exposure to the metal in the form of fumes or dust. Hazards for the general population, including newborn and developing children, and other living organisms may also originate from prolonged low-level exposure to manganese and its organometallic compounds released into the environment as a result of their variety of applications. Experimental evidence has been presented to show that developing mice and rats are not able to excrete manganese for first 17-18 days of life, with excessive tissue accumulation, and their brain is more susceptible to the neurotoxic effects of manganese. Prolonged exposure to manganese causes depletion of dopamine and other monoamines in adult rats. The short-term exposure produces an increase in the binding of dopaminergic antagonist [3H]-spiroperidol to striatal membranes without affecting the other neurotransmitter receptors at low doses (10 mg/kg X 15). A higher dose (15 mg/kg X 15), causes a decrease in cerebral GABA, frontal cortical serotonin and striatal muscarinic binding and an increase in binding of [3H]-spiroperidol to striatal membranes. No significant changes occur in the levels of dopamine or serotonin at either of these two doses. The neonatal rat in certain respects shows a different effect on dopamine levels and receptor sensitivity. Exposure to manganese causes an increase in levels of dopamine and norepinephrine. Neonatal exposure to manganese (10 mg/kg X 15) produces a decrease in binding of [3H]-spiroperidol to striatal membranes and of serotonin to frontal cortical membranes.

Aging↗
PubMed1996

[A patient with parkinsonism presenting hyperintensity in the globus pallidus on T1-weighted MR images: the correlation with manganese poisoning].

We report a 55-year-old woman who developed symptoms resembling parkinsonism. Her psychiatric symptoms in the early stage, cervical dystonia and tremor increasing on movement were consistent with manganese poisoning. Manganese levels were elevated to 1.5 micrograms/l in the serum (normal; 0.3-1.1 micrograms/l) and to 1.4 micrograms/l in the urine (normal; less than 1.2 micrograms/l). Intravenous infusion of calcium disodium editate (CaEDTA; chelating agent) was followed by the marked excretion of manganese (27.3 micrograms/l) in the urine. These findings support manganese poisoning. Manganese poisoning is a disease which results from chronic exposure to manganese, but the source of manganese exposure remained obscure in this patient. T1-weighted MRI of the brain showed symmetric high signal intensity in the globus pallidus without any abnormality on T2-weighted images. There is a report that manganese induced brain lesions in Macaca fascicularis as revealed by MRI and the fascicularis developed signs of unsteady gait and hypoactivity. The patient responded to treatment with CaEDTA and the second MRI demonstrated regression of abnormal signal intensity. This may be due to enhanced manganese excretion. To our knowledge, this is the first case of probable manganese-induced human parkinsonism whom changes in MRI were noted after treatment with CaEDTA.

Edetic Acid↗
PubMed1987

Manganese poisoning and the attack of trivalent manganese upon catecholamines.

Human manganese poisoning or manganism results in damage to the substantia nigra of the brain stem, a drop in the level of the inhibitory neurotransmitter dopamine, and symptoms resembling those of Parkinson's disease. Manganic (Mn3+) manganese ions were shown to be readily produced by O-2 in vitro and spontaneously under conditions obtainable in the human brain. Mn3+ as its pyrophosphate complex was shown to rapidly and efficiently carry out four-electron oxidations of dopamine, its precursor dopa (3,4-dihydroxyphenylalanine), and its biosynthetic products epinephrine and norepinephrine. Mn3+-pyrophosphate was shown to specifically attack dihydroxybenzene derivatives, but only those with adjacent hydroxyl groups. Further, the addition of Mn2+-pyrophosphate to a system containing a flux of O2- and dopamine greatly accelerated the oxidation of dopamine. The oxidation of dopamine by Mn3+ neither produced nor required O2, and Mn3+ was far more efficient than Mn2+, Mn4+ (MnO2), O2-, or H2O2 in oxidizing the catecholamines. A higher oxidation state, Mn(OH)3, formed spontaneously in an aqueous Mn(OH)2 precipitate and slowly darkened, presumably being oxidized to MnO2. Like reagent MnO2, it weakly catalyzed dopamine oxidation. However, both MnO2 preparations showed dramatically increased abilities to oxidize dopamine in the presence of pyrophosphate due to enhancement of the spontaneous formation of the Mn3+ complex. These results strongly suggest that the pathology of manganese neurotoxicity is dependent on the ease with which simple Mn3+ complexes are formed under physiological conditions and the efficiency with which they destroy catecholamines.

Catecholamines↗
PubMed1986

[Effect of manganese poisoning on the levels of manganese and iron in rat viscera].

Twenty rats were poisoned by manganese inhalation, and sacrificed six months after the first exposure. The tissue concentrations (in microgram/g dry weight) of manganese and iron were found in liver, pancreas, lung, kidney and suprarenal gland for atomic absorption spectrometry in control and experimental animals. The measurements show high tissue concentrations of manganese, especially in liver and pancreas of the experimental animals, as well as a little increase in the tissue concentrations of iron, fundamentally in liver, kidney and suprarenal gland.

Adrenal Glands↗
PubMed1986

Chronic manganese poisoning: a neuropathological study with determination of manganese distribution in the brain.

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.

Aged↗
PubMed1986

[Levels of manganese and iron in the brain of normal and manganese-poisoned rats].

Forty rats were poisoned by manganese inhalation and were sacrificed after six and nine months. Tissue concentrations (in mg/g dry weight) were measured in brain, cerebellum and stem-brain of the experimental animals and the twenty control rats, for atomic absorption spectometry. The increase in tissue manganese concentrations were very pronounced in cerebellum, and minor in brain and stem-brain. The tissue iron concentrations undergo a light increase in cerebellum and stem-brain.

Animals↗
PubMed2003

Behavioral impairments in acute and chronic manganese poisoning in white rats.

Single p.o. doses of manganese chloride (MnCl2 x 4H2O; 50 mg/kg) induced significant and reversible decreases in total activity in white rats, along with worsening of the acquisition of an avoidance reaction in response to unconditioned and conditioned stimuli, increases in the latent period of conditioned reflex activity, and a temporary worsening of the learning process. Chronic manganese poisoning (daily p.o. manganese chloride at 20 or 50 mg/kg for one month) led to significant impairment of learning processes in a multipath maze but had no significant effect on reproduction of previously acquired stereotypical behavior.

Animals↗
PubMed1992

A report of two cases of chronic serious manganese poisoning treated with sodium para-aminosalicylic acid.

Two cases of chronic manganese poisoning were treated with sodium para-aminosalicylic acid (PAS-Na; 6 g/day in 500 ml of 10% glucose solution by intravenous drip). The results indicated that one had been clinically cured and that the other had obviously improved in clinical symptoms and signs. Thus PAS-Na appears to be an effective drug for treatment of serious chronic manganese poisoning.

Aminosalicylic Acid↗
PubMed1980

Haematological responses in a fresh water fish to experimental manganese poisoning.

Blood dyscrasia in a fish exposed to experimental manganese poisoning is described. Colisa fasciatus, a fresh water teleost, showed significant decreases in the total erythrocyte count, number of erythrocytes/1000 blood cells of all types, and in the hepatosomatic index (relative liver wt) after exposure for 90 h to 2500 mg/l manganese sulphate; the 96 h LC50 value was 2850 mg/l. The exposure also evoked leucocytosis due to an increase in the number of small lymphocytes. Other haematological characteristics, viz., total count of thrombocytes, distribution of immature red blood cells, thrombocytes and large lymphocytes/1000 blood cells, haematocrit, erythrocyte sedimentation rate, haemoglobin, and clotting time, did not differ significantly from the controls.

Anemia↗