Objective: To explore the changes of γ-GCS mRNA expression and GSH-PX in serum of workers exposed to manganese in order to provide scientific basis for early diagnosis of manganese poisoning. Methods: In June 2017, a total of 180 workers from a motorcycle manufacturer were selected by stratified random sampling, including 115 welders as the exposure group and 65 administrative office workers as the Control Group, the exposure group was divided into high exposure group (43 persons) and low exposure group (72 persons) according to whether the exposure group exceeded the standard limit. The levels of γ-gcs Mrna expression and GSH-Px activity in serum were determined by Occupational Health Survey, and the differences of γ-gcs Mrna expression and GSH-Px activity among different groups were analyzed. Results: Compared with the control group, the serum GSH-Px activity was lower and the serum γ-GCS mRNA expression level was higher in the exposed group (F=370.52, 275.95, P<0.01) . Compared with the control group, there was significant difference in γ-GCS mRNA expression level and GSH-Px activity (F=0.475、1.06, P<0.01; F=48.53、111.70, P<0.01) . The concentrations of manganese in air, welding dust and urine were positively correlated with the level of γ-GCS mRNA (r=0.71, 0.50, 0.31, P<0.01) The serum GSH-Px activity was negatively correlated with the concentrations of manganese in air, welding dust and urine (r=-0.80, -0.52, -0.30, P< 0.01) , There was no correlation between Serum γ-GSH-Px activity and age and years of exposure (P>0.05) . Conclusion: Serum γ-GCS mRNA expression level and GSH-Px activity level can be used as early biomarkers of manganese poisoning. The concentrations of manganese in workplace air, welding dust and urine manganese in workers are the influencing factors.
Air Pollutants, Occupational ; Dust ; Humans ; Ions ; Manganese ; Manganese Poisoning ; Occupational Exposure/analysis* ; RNA, Messenger/genetics* ; Welding

Long-term occupational exposure to manganese might cause manganese poisoning, which would had adverse effects on nervous system of workers. The basal nucleus was damaged and dopaminergic neuron was injuried by manganese. The mechanism could be related with interfering the energy metabolism of central nerve, changing neurotransmitters, activating oxidation system and so on. Genetic factors may also plays a significant role in the neurotoxicity caused by manganese. Study the effects of manganese exposure biomarker, the neurotoxicity of biomarkers and the genetic susceptibility to early and susceptibility biomarkers will contribute to the prevention and control of manganese neurotoxicity.
Biomarkers ; Disease Susceptibility ; Humans ; Manganese ; Manganese Poisoning ; Neurotoxicity Syndromes ; Occupational Exposure

OBJECTIVETo investigate the effects of polygala on leaning and memory and the expression of Microtubule associated protein on manganese poisoned mice.

METHODS60 female Kunming mice were randomly and equally divided into 5 group. They are normal control group (CG), manganese poisoned group (MG), manganese poisoned with polygala high dose group (MHG), manganese poisoned with polygala middle dose group (MMG), manganese poisoned with polygala low dose group (MLG). The model of manganese poisoned mice was prepared of the way of intraperitoneal injection of manganese chloride (MnCl2 15 mg/kg), the spatial learning and memory ability was tested by Morris water maze, the Doublecortin (DCX) was tested by the way of immunofluorescent staining in the SVZ and SGZ.

RESULTIn the navigation test, compared with MG, the escape latency of MHG, MMG and MLG were significantly decreased (P < 0.05), in space exploration experiments, MHG, MMG, MLG compared with MG, the number increased significantly across platforms (P < 0.05). compared with MG, the DCX expression of MHG, MMG and MLG were significantly increased (P < 0.05).

CONCLUTIONThe leaning and memory ability of manganese poisoned mice can be improved by the polygala, and the mechanism may be related to promote the expression of DCX and neurogenesis in the brain.

Animals ; Female ; Manganese Poisoning ; drug therapy ; Maze Learning ; drug effects ; Memory ; drug effects ; Mice ; Microtubule-Associated Proteins ; drug effects ; Neurogenesis ; drug effects ; Neuropeptides ; drug effects ; Plant Extracts ; pharmacology ; Polygala ; chemistry

Cognition Disorders ; chemically induced ; Humans ; Manganese ; toxicity ; Manganese Poisoning ; epidemiology

OBJECTIVETo investigate the relationship between mRNA expression of manganese superoxide dismutase (MnSOD) and manganese neurotoxicity.

METHODSThirty-one patients with occupational chronic manganese poisoning (case group), as well as 31 controls exposed to the same condition (control group), were included in the study. Whole blood RNA was extracted, and the mRNA expression of MnSOD was measured by RT-PCR; the two groups were compared in terms of the mRNA expression of MnSOD. PC12 cells were treated with 0, 100, 200, 400, 600, 800, and 1000 ümol/L MnCl₂ for l, 2, 3, and 4 d; the cell viability was determined by MTT assay, and the mRNA expression of MnSOD was measured by RT-PCR.

RESULTSThe case group had significantly lower mRNA expression of MnSOD than the control group (0.390 ± 0.080 vs 0.582 ± 0.219, P < 0.05). MnCl2 had a toxic effect on PC12 cells; the concentration of MnCl₂ was positively correlated with the toxic effect but negatively correlated with the mRNA expression of MnSOD.

CONCLUSIONMnSOD mRNA may be involved in the manganese-induced damage of nerve cells. It is hypothesized that high mRNA expression of MnSOD may play an inhibitory effect on manganese neurotoxicity.

Adult ; Animals ; Female ; Gene Expression ; Humans ; Male ; Manganese Poisoning ; genetics ; Middle Aged ; Neurotoxicity Syndromes ; genetics ; PC12 Cells ; RNA, Messenger ; genetics ; Rats ; Superoxide Dismutase ; genetics

OBJECTIVETo investigate the effects of enriched environment and impoverished environment on the learning and memory ability of manganese-exposed mice and the mechanism.

METHODSForty female Kunming mice were randomly and equally divided into 4 group: control group (CG), standard environment and manganese exposure group (SEG), enriched environment and manganese exposure group (EEG), and impoverished environment and manganese exposure group (IEG). The mouse model of manganese poisoning was established by intraperitoneal injection of manganese chloride. The learning and memory ability was tested by Morris water maze. The expression of cAMP response element-binding protein (CREB) in area CA1 of the hippocampus was measured by immunohistochemistry.

RESULTSIn place navigation test, the SEG had a significantly longer escape latency than the CG (P < 0.05), and the EEG had a significantly shorter escape latency than the SEG (P < 0.05); there was no significant difference in escape latency between IEG and SEG (P > 0.05). In spatial probe test, the EEG had a significantly greater number of platform crossings than the SEG (P < 0.05), and the IEG had a significantly smaller number of platform crossings than the SEG (P < 0.05). The expression of CREB in area CA1 of the hippocampus was significantly lower in IEG and SEG than in CG (P < 0.05), and it was significantly higher in EEG than in SEG (P < 0.05).

CONCLUSIONIn the enriched environment, the learning and memory ability of manganese-exposed mice can be improved, which may be due to the increased expression of CREB in the hippocampus.

Animals ; Cyclic AMP Response Element-Binding Protein ; metabolism ; Disease Models, Animal ; Environment ; Female ; Hippocampus ; drug effects ; metabolism ; Learning ; drug effects ; Manganese Poisoning ; metabolism ; Memory ; drug effects ; Mice

Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.
Arsenic ; Ataxia ; Carbon Disulfide ; Carbon Monoxide ; Cerebellar Diseases ; Delivery of Health Care ; Developing Countries ; Dimethylamines ; Disease Outbreaks ; Electrophysiology ; Gases ; Hexanes ; Hydrogen Sulfide ; Manganese ; Metals, Heavy ; Nervous System ; Neuroimaging ; Neurologic Manifestations ; Neuromuscular Junction Diseases ; Neurotoxins ; Occupational Diseases ; Occupational Health ; Organophosphate Poisoning ; Organophosphates ; Parkinsonian Disorders ; Polychlorinated Biphenyls ; Quaternary Ammonium Compounds ; Semiconductors ; Sodium Fluoride ; Solvents ; Taiwan ; Thallium ; Tin ; Toluene ; Urethane

Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.
Arsenic ; Ataxia ; Carbon Disulfide ; Carbon Monoxide ; Cerebellar Diseases ; Delivery of Health Care ; Developing Countries ; Dimethylamines ; Disease Outbreaks ; Electrophysiology ; Gases ; Hexanes ; Hydrogen Sulfide ; Manganese ; Metals, Heavy ; Nervous System ; Neuroimaging ; Neurologic Manifestations ; Neuromuscular Junction Diseases ; Neurotoxins ; Occupational Diseases ; Occupational Health ; Organophosphate Poisoning ; Organophosphates ; Parkinsonian Disorders ; Polychlorinated Biphenyls ; Quaternary Ammonium Compounds ; Semiconductors ; Sodium Fluoride ; Solvents ; Taiwan ; Thallium ; Tin ; Toluene ; Urethane

Adult ; Aminosalicylic Acid ; therapeutic use ; Female ; Humans ; Manganese Poisoning ; drug therapy

OBJECTIVETo study the relationship between polymorphisms of MnSOD and the susceptibility of chronic poisoning exposed to manganism occupationally.

METHODSIn a study of case-control, genotypes were determined by PCR-RFLP in 164 patients with chronic occupational mangamism poisoning and 328 controls with age- and sex-matched for MnSOD 9Ala-Val.

RESULTSThere was a significant difference in the frequency of MnSOD 9Ala-Val at V locus mutant allele between cases and controls (χ(2) = 15.225, P < 0.01, 95%CI = 1.43 ∼ 3.00). Individuals with the genotype VV had a 1.30 of risk increase of occupational chronic manganism poisoning compared with the the genotype AV or AA (OR = 2.30, 95%CI = 1.52 ∼ 3.49, P < 0.05).

CONCLUSIONThe MnSOD polymorphisms may be related with the susceptibility to chronic occupational manganism poisoning, the risk of chronic occupational manganism poisoning increases in carriers with genotype VV at MnSOD 9Ala-Val locus.

Adult ; Case-Control Studies ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Manganese Poisoning ; genetics ; Middle Aged ; Occupational Diseases ; genetics ; Occupational Exposure ; Polymorphism, Single Nucleotide ; Superoxide Dismutase ; genetics