The obtained results suggest that prior exposure to manganese may have attenuated the effects of inhalation exposure to manganese in adulthood, in which the expression of inflammation-related genes were suppressed. Studies of the neuropathological bases for manganese neurotoxicity have pointed to the involvement of the corpus striatum and the extrapyramidal motor system (Archibald and Tyree, 1987, Eriksson et al., 1987; 1992). In vitro exposure to MnCl2 (0.2–2.0 mM) produced a dose-dependent increase in the formation of ROS (Ali et al., 1995). May cause central Another study by Dorman et al.   Mn-SOD is primarily located in mitochondria, which play an important role in scavenging superoxide radicals (Weisiger and Fridowich,1973). occur. The biochemical mechanisms underlying the interaction between Mn and other minerals are unclear. Danger! CT scans are not useful diagnostically, but MRI reveals increased signal on T1-weighted images within the basal ganglia. Total SOD, Cu,Zn-SOD, and Mn- SOD activities in different regions of the brains of control and Mn-treated rats are presented in Figs. Manganese poisoning has been linked to impaired motor skills and cognitive disorders. These changes were observed both when the animals were exposed while in utero or postpartum. In toxic concentrations, the detrimental effects of Mn on human health include childhood developmental disorders and manganism. Manganese (CAS registry number 7439-96-5) makes up about 0.10% of the earth's crust and is the 12th most abundant element. Yes, manganese dioxide is toxic, you must put it in a higher and not dangerous place. Limited evidence suggests that dopamine levels in caudate nucleus and putamen are decreased in affected patients (Bernheimer et al., 1973). Manganese is an essential mineral. Mn was also found to decrease DA uptake and DA efflux in DAT-transfected human embryonic kidney cells by promoting redistribution of DAT from the cell surface to the internal compartment of the cell (Roth et al., 2013). Therefore, all toxicity studies described here are chronic in nature. W. Michael Caudle, in Handbook of Clinical Neurology, 2015. Catalog Numbers: Synonyms. Carbon monoxide and other minerals cause manganese toxicity to have a worse tremor, according to the library work. MnO2 induces pathological reactions in the lung via cellular elements normally present in the lungs. The primary source of this element is food; fruits, nuts, grains, and vegetables are all rich in Mn.107, Mn has replaced lead as a fuel additive and is used in fertilizers and in the manufacture of fireworks. Headache, irritability, and memory disturbance can be seen with acute or chronic Mn encephalopathy. Manganese dioxide. Ingestion or inhalation of large amounts of manganese will cause a disease called manganism. Manganese dioxide nanomaterial is a new type of inorganic nanomaterial offering numerous advantages: simple preparation, low cost, and environmental friendliness. These results suggest that manganese-induced neurotoxicity may be mediated via generation of ROS. However, while most studies report the preservation of dopaminergic regions, such as the caudate, putamen, and substantia nigra (Shinotoh et al., 1995; Olanow et al., 1996; Pal et al., 1999; Olanow, 2004), others suggest a mild damage to these regions as well as a general alteration in their function following manganese exposure (Suzuki et al., 1975; Eriksson et al., 1992; Kim et al., 2002; Chen et al., 2006; Wright et al., 2004; Guilarte et al., 2006; Criswell et al., 2011). The central nervous system is the primary target. and bronchitis and susceptibility to infectious lung disease. Many developmental toxicity studies in animals exposed to Mn have focused on possible effects on reproductive and neurological functions. (1999), in which reaction oxygen species in the brains of neonatal rats administered up to 22 mg/manganese/kg/day for up to 49 days were followed, also did not support the hypothesis that oxidative damage is a mechanism of action in manganese-induced neurotoxicity in rat. Final Report: Nanofibrous Manganese Dioxide for Volatile Organic Compounds EPA Contract Number: 68D02027 Title: Nanofibrous Manganese Dioxide for Volatile Organic Compounds Investigators: Xiao, Danny Small Business: Inframat Corporation EPA Contact: Richards, April Phase: I Project Period: April 1, 2002 through September 1, 2002 Project Amount: $70,000 Special hazards arising from the substance or mixture Manganese/manganese oxides. Animal studies have shown that Mn exposure decreased the growth of reproductive organs (preputial gland, seminal vesicle and testes) (Gray and Laskey, 1980). ... literature, biological activities, safety/hazards/toxicity information, supplier lists, and more. Inhalation of fumes may cause metal-fume (1993) demonstrated reduced body weight of mice during development after exposure to 8 or 16 mg/kg Mn (II). Early symptoms include sluggishness, sleepiness, and weakness in the legs.   Further studies using imaging techniques have identified significant reductions in the dopaminergic D2 receptor in the basal ganglia. The hallmark of PD is the degeneration of the nigrostriatal DAergic neurons in the substantia nigra pars compacta that innervate the caudate and putamen. May cause eye irritation. Manganese Essentiality, transporting characteristics and toxicity of manganese Manganese (Mn) is a trace metal commonly found in the environment. Manganese Dioxide Safety Data Sheet according to Federal Register / Vol. 86.94 Molecular Formula. AC203191000, AC203195000, AC213490000, AC213490010, AC213490250, SAFETY DATA SHEET Creation Date 26-Feb-2010 Revision Date 17-Jan-2018 Revision Number 4 1. The substantia nigra is sometimes affected but generally to a lesser extent (Katsuragi et al., 1996; Yamada et al., 1986). ), the univalent reduction product of dioxygen (Coassin et al., 1992; Singh et al., 1992; Tampo and Yonaha, 1992). Manganese or potassium ignites in nitrogen dioxide [Ann. (1999) demonstrated atypical antioxidative properties of manganese in iron-induced brain lipid peroxidation and copper-dependent low-density lipoprotein conjugation, but the underlying mechanisms of the antioxidant effects are not clear. It is important in building bone, healing wounds, and in how the body uses carbohydrates and amino acids.   Chronic Exposure: Chronic manganese poisoning can result from excessive inhalation and ingestion exposure and involves impairment of the central nervous system. Liccione and Maines (1988) reported decreased levels of CAT, GSH, and GPx activities in rat striatum exposed to Mn. 4 ; H332 - For the full text of the H -Statements mentioned in this Section, see Section 16. In 13-week dietary studies, no gross or histopathological lesions or organ weight changes were observed in reproductive organs of rats fed up to 618 mg Mn/kg/day or mice fed up to 1950 mg Mn/kg/day.   Up to 5% is required. 1 Reagent Lane Chronic manganese poisoning can result from excessive inhalation and ingestion exposure and involves impairment of the central nervous system.   Studies in Caenorhabditis elegans have shown that Mn has the ability to induce DAergic-specific neurodegeneration. Most common were nausea (7%), headache (4%), vomiting and abdominal pain (2% each), chest pain and palpitation (1% each), and hypertension, flushing, vasodilatation, and hypotension (under 1% each).   Their study showed that oral Mn exposure (11 or 22 mg/kg/day for 21 days) induced a significant increase in amplitude of the acoustic startle reflex and an increase in striatal DA and 3,4-dihydroxyphenylacetic acid concentrations in neonates treated with high doses. Although manganese exposure can occur through several different forms, including ingestion of food and exposure to manganese-containing products, exposure in an occupational setting such as mining, smelting, and welding appears to be a major contributor to these toxicants. Other chronic effects from inhaling 0.2 mg/m3 TWA (as Mn) (listed under Manganese, inorganic compounds). The formation of ROS was higher in younger animals as compared to older animals. are present, they tend to continue and worsen after exposure ends. Uses advised against Not for food, drug, pesticide or biocidal product use Details of the supplier of the safety data sheet An increased expression of Mn-SOD may serve to protect the mitochondria from the toxic effects of superoxide radicals that are generated due to Mn accumulation.   Harmful if inhaled. In terms of the neurochemistry of manganese toxicity, some other studies have shown that dopamine levels are affected by manganese exposure in humans, monkeys, and rodents, with various indications of an initial increase in dopamine followed by a longer-term decrease (Barbeau, 1984; Donaldson, 1984). Oxidative stress generated through mitochondrial perturbation may be a key event in the demise of the affected central nervous system cells. Early symptoms include sluggishness, sleepiness, and weakness in the legs. Aspiration may cause severe pneumonia. By continuing you agree to the use of cookies. It can exist in oxidation states from -3 to +7, the most common being +4 in the chemical form of manganese dioxide (Keen and Leach 1988). Most common source of manganese in glazes.   When exposure to manganese occurred during gestation, the extent of altered gene expression induced by subsequent exposure to manganese in adulthood was reduced. Manganese dioxide, when found in nature, is known as pyrolusite. Manganese Dioxide tech CAS No 1313-13-9 MATERIAL SAFETY DATA SHEET SDS/MSDS. Black manganese oxide; Manganese dioxide; Manganese(IV) oxide; Chronic inhalation exposure appears to have a poor prognosis from the standpoint of the encephalopathy and motor symptoms, but tremor does tend to improve some. After withdrawal of manganese the symptoms all disappeared. To date, there is no conclusive experimental evidence for how and if this process impacts microbial fitness in the environment. The GSH content was expressed as nmol/mg of protein; mean ± SEM for 6–8 animals per age group. Urine or stool levels provide better means of assessing potential toxic exposure. This practice obviously puts workers at risk to the toxic effects of the dust. 1946-47]. Concentrated nitric acid reacts with manganese with incandescence and a feeble explosion [Mellor 12:188. It is considered to be the most plentiful out of all the manganese compounds. There are reports that suggest that increased expression of Mn-SOD plays a central role by diminishing oxygen-mediated injuries and the cytotoxic effects of various toxicants and therapeutic agents (Hirose et al., 1993; Cobbs et al., 1996). Clinical signs of toxicity include reduced appetite and growth rate, anemia and abdominal discomfort.   Chronic: through the intestine, inorganic manganese salts may produce   1946-47]. Manganese peroxide; Manganese binoxide; Manganese black; Battery updated fri 17 nov 00 : vince pitelka on mon 13 nov 00 This has come around many times on Clayart, but it is important to mention it again whenever anyone asks. The role of mitochondrial energy metabolism in manganese toxicity was indicated by two studies (Aschner and Aschner, 1991; Gavin et al., 1990). 58 / Monday, March 26, 2012 / Rules and Regulations 02/26/2015 EN (English) 3 Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. (2011, 2012) found the pallidal nuclei to be more susceptible to manganese accumulation compared with the caudate and putamen in welders with high occupational exposure to manganese. nausea, vomiting and diarrhea. Early symptoms include languor, sleepiness and weakness in the legs. In young children, however, even limited exposures have been shown to produce long-term developmental delays.113–116, EEG studies are typically normal in cases of Mn poisoning. A portion of manganese probably exists in the synaptic vesicles in glutamatergic neurons, and manganese is dynamically coupled to the electrophysiological activity of the neurons. May cause respiratory tract irritation. In high concentrations, Mn causes an irreversible brain disorder with prominent psychologic and neurologic disturbances (Aschner and Aschner, 1992). Manganese exposure in miners and during processing of manganese ore and ferromanganese is known to cause an extrapyramidal syndrome characterized by progressive parkinsonism, dystonia, and neuropsychiatric symptoms. Decomposes to MnO at 1080C. no grain cereals, nuts, or blueberries). 10). However, a study by Sziraki et al. (2000) also suggested that neonatal rats are at greater risk than adults for Mn-induced neurotoxicity when compared under similar exposure conditions. AC193470000, AC193470050, AC203190000, AC203190030, AC203190050, There are no reports of acute toxicity of Mn in animals. Manganese dioxide also catalyses the decomposition of hydrogen peroxide to oxygen and water: 2 H 2 O 2 → 2 H 2 O + O 2. In addition to these well-established neurotoxic effects, Mn has been extensively studied for its reproductive and developmental effects. similar to those of Parkinson's disease. and in lettuce [Lactuca saliva L.] (1, 2, 3). Tremor, dysarthria, increased tone, and gait disturbance occur relatively late in the process.110,112,113, Recovery from toxicity depends somewhat on the duration and form of exposure but tends to be slow and minimal. A diet can be consumed without any adverse effect when the Mn level is 2000 ppm for calves, 3000 ppm for sheep, 3000 ppm for chickens, 4000 ppm for turkeys and 7000 ppm for rats. Total SOD activities did not vary significantly in any region of the brain examined. is … Insoluble in water. The authors concluded that exposure to mangafodipir trisodium is not associated with short-term risks. Mn is considered to be one of the least toxic of the essential elements (NRC, 2005). Synonyms: It functions as General description. Individuals with poor hepatic function are at increased risk of Mn toxicity due to decreased excretion of the metal.109 Once in the brain, it accumulates in gray matter. Neuropathological findings include cell loss in the globus pallidus, putamen, caudate, and substantia nigra.8, Rapid elimination from the blood limits the usefulness of serum Mn levels in diagnosis. Both patients had mild headache and dizziness. The highest concentrations in normal brains are found in the melanin-rich globus pallidus and striatum.110,111 The neurotoxicity of Mn is thought to result from potentiation of free radical production and apoptosis.90,112, The classic and most prominent manifestation of Mn toxicity is parkinsonism, but encephalopathy also occurs with both acute and chronic exposures. lungs may occur is still unknown. The specific area of injury in humans seems to be primarily in the globus pallidus.   Studies in neonatal animals have detected structural and neurochemical changes at doses of Mn similar to or slightly above dietary levels (1–10 mg Mn/kg/day) (Chandra and Shukla, 1978; Deskin et al., 1980), suggesting that young animals might be more susceptible to Mn than adults. Figure 13. Impaired fertility was observed in male mice exposed to Mn in drinking water for 12 weeks at a daily dose level of 309 mg/kg/day, but not at doses ≤154 mg/kg/day (Elbetieha et al., 2001). Manganese can be found in the iron ores used by the Spartans. This suggests the possibility of mitochondria being a critical site for Mn toxicity. Ingestion or inhalation of large amounts of manganese will cause a disease called manganism. et Phys. Inhalation: The brain normally contains a small amount of Mn (Cotzias et al., 1968). May cause gastrointestinal irritation with reproductive system. Manganese Other name(s) Manganese citrate, manganese gluconate, manganese sulfate. The general, Toxic Encephalopathies I: Cortical and Mixed Encephalopathies, Handbook on the Toxicology of Metals (Third Edition), , understanding the movement and action of manganese in synapses may be important to clarify the function and, Dorman et al., 2006; Guilarte et al., 2006, Butterworth, Spahr, Fontaine, & Layrargues, 1995; Mousseau, Perney, Layrargues, & Butterworth, 1993; Sriram, Lin, Jefferson, Roberts, Chapman, et al., 2010, Brouillet, Shinobu, McGarvey, Hochberg, & Beal, 1993, Benedetto, Au, Avila, Milatovic, & Aschner, 2010, Schroeder et al., 1966; Hurley et al., 1984; Golub et al., 2005, Tjalve and Henriksson, 1999; Vitarella et al., 2000; Fechter et al., 2002; Normandin et al., 2004, Brenneman et al., 2000; Aschner et al., 2005, Gorell et al., 1999a, b; Racette et al., 2012, Semchuk et al., 1993; Seidler et al., 1996; Marsh and Gula, 2006, Shinotoh et al., 1995; Olanow et al., 1996; Pal et al., 1999; Olanow, 2004, Suzuki et al., 1975; Eriksson et al., 1992; Kim et al., 2002; Chen et al., 2006; Wright et al., 2004; Guilarte et al., 2006; Criswell et al., 2011, Maynard and Cotzias, 1955; Brouillet et al., 1993; Gavin et al., 1999, Dukhande et al., 2006; Erikson et al., 2008, Handbook of Developmental Neurotoxicology, Reproductive and Developmental Toxicology (Second Edition), Neurotoxicity of Nanomaterials and Nanomedicine. Strong oxidizer. Thus, it is a very potential new material for the preparation of catalytic micromotors, but has been scarcely explored to … Manganese released into the synaptic cleft may influence synaptic transmission. Manganese dioxide will release chlorine gas in contact with hydrochloric acid. The reasons for this controversy are varied, suggesting that this is an area that needs further investigation. Potential Health Effects Manganese is concentrated in the mitochondria of cells. In Meyler's Side Effects of Drugs (Sixteenth Edition), 2016. In contrast, the most significant effects of Mn toxicity occur at the globus pallidus, while synthesis of DA and DAT levels in the substantia nigra is preserved in most cases (Yamada et al., 1986). For International CHEMTREC assistance, call: 703-527-3887. MnO 2. Pyrolusite is the principal ore of the compound manganese dioxide. Abbreviations: C, control; 2.5 mg MnCl2/kg ip; 5 mg MnCl2/ kg ip. Mn-SOD activity was not altered in the caudate nucleus or frontal cortex, however, there was a significant increase of Mn-SOD activity in the hippocampus (Fig. Figure 10. The GPx activity is expressed as mU/mg of protein; mean ± SEM for 6–8 animals per group. Revised on 07/30/2012 Page 1 of 6 Safety Data Sheet Manganese Dioxide, Fine Granular Reagent 1. Effect of manganese on glutathione peroxidase activity in different regions of rat brain. cause eye, skin, and respiratory tract irritation. Mn crosses the blood–brain barrier in both the adult and the developing fetus. Company Identification: Using an exposure paradigm that closely mimics that seen in humans, pathology appeared to be preferential for the globus pallidus, while leaving the dopaminergic inputs relatively untouched. It is used in iron and steel manufacturing, in metal-finishing operations, and as an alloy in welding.90,108 The most common setting of toxic Mn exposure is occupational. Both Mn(III) and Mn(II) can cross the blood–brain barrier, although it is suggested that Mn(III) is predominantly transported bound to the protein transferrin, whereas Mn(II) may enter the brain independently of such a transport mechanism (Murphy et al., 1991). It is needed by the body in very small amounts. Miners and welders are at the highest risk of manganese toxicity. Effect of manganese on glutathione content in different regions rat brain. The general toxicity of manganese [7] and its neurotoxicity [8] have been reviewed. The association between elevated occupational exposure to manganese and neurobehavioral and motor dysfunction has been understood since the 1830s, when James Couper first described a neurologic dysfunction that shared many similarities to PD in workers exposed to manganese ore. Interestingly, at this time, Couper was able to delineate the symptomology related to manganese exposure that was distinct from typical PD. Patients should be carefully monitored when receiving long-term parenteral nutrition including manganese, even when the manganese dose is small and administration infrequent. MSDS Name: Manganese(IV) dioxide Fair Lawn, NJ 07410 The CNS of neonatal rats was found to be more susceptible to Mn-induced neurotoxicity compared with the adult rat CNS (Kontur and Fechter, 1988). Abbreviations: C, control; 2.5 mg MnCl2,/kg ip; 5 mg MnCl2,/kg ip.   Manganese dioxide | MnO2 | CID 14801 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more. Inhalation of particulate manganese compounds such as manganese dioxide (MnO 2 ) or manganese tetraoxide (Mn 3 O 4 ) can lead to an inflammatory response in the lung. Studies also show that Mn-SOD is altered whereas other antioxidative enzymes such as Cu-Zn SOD and GPx remain unchanged (Hussain et al., 1997a). Since these findings, reports relating manganese exposure with parkinsonism have been mixed, with some studies identifying a clear association with occupational exposure (Gorell et al., 1999a, b; Racette et al., 2012), while others have not identified a similar link (Semchuk et al., 1993; Seidler et al., 1996; Marsh and Gula, 2006). CNS depression.   Manganese is an essential trace element in humans that can elicit a variety of serious toxic responses upon prolonged exposure to elevated concentrations either orally or by inhalation. For information, call: 201-796-7100 Significant differences across the different groups were evaluated by ANOVA, and p values (< 0.05) are indicated (*) on the top of the bars. In view of the biologic role of Mn, there are several possibilities that may explain the increasing levels of Mn-SOD activity. Mn can have a damaging effect on many body organs, including the brain, liver, pancreas and reproductive system. RTECS # OP0350000 CAS # ... July 2015 Molecular Weight. 10 and 11). Developmental studies involving the use of laboratory animals have also detected subtle changes in growth (decreased body weight in animals provided with relatively high doses of Mn). In all domestic animals and poultry, excess dietary Mn is known to cause reduced feed intake, growth rate, and lethargy. A large portion of manganese is bound to manganese metalloproteins, especially glutamine synthetase in astrocytes. Manganese Dioxide is commonly used for batteries and also as pigment for other Manganese … Formation of Mn(III) may occur by oxidation of Mn(II) by superoxide (Hussain et al., 1997). After being taken up, manganese is retrogradely transported to the cell body, where it can be released into the interstitial space (Tjalve and Henriksson, 1999; Vitarella et al., 2000; Fechter et al., 2002; Normandin et al., 2004). It is essential for maintaining the proper function and regulation of many bio-chemical and cellular reactions [1]. Warner et al. Eye: Treatment is generally limited to removal of the toxic source, but chelation with calcium–ethylenediaminetetraacetic acid has shown some benefit in cases of acute exposure. On the other hand, Intrastriatal Mn injections in the rat brain have been found to cause DAergic neuron loss (Brouillet, Shinobu, McGarvey, Hochberg, & Beal, 1993). Available human toxicity data are limited to the industrial setting, where adverse health effects have resulted from inhalation of manganese (primarily as manganese dioxide). The toxic effects of manganese in dogs [5] and humans [6] tend to involve the heart, liver, and nervous system, but some endocrine effects can occur. Organic Mn crosses the BBB by passive diffusion. Mn neurotoxicity causes an extrapyramidal motor disorder that resembles idiopathic PD. Chronic manganese poisoning primarily involves the central nervous system.   (1993) suggested that the mitochondrial dysfunctional effects of manganese result in various oxidative stress to cellular defense mechanisms and secondary free radical damage to mitochondrial DNA. In one case, manganese had been given once or twice a week for 4 years and in the other case twice a month for 5 years. Attempts to chelate manganese with CaNa2EDTA have not been successful. Abbreviations: C-control; 2.5 mg MnCl2,/kg, ip; 5 mg MnCl2,/kg ip,. Manganese dioxide   Manganese is another essential metal with important functions in multiple biologic processes, including serving as cofactors for enzymes, including superoxide dismutase, as well as participating in neurotransmitter metabolism (Schroeder et al., 1966; Hurley et al., 1984; Golub et al., 2005). The toxic effects of manganese in dogs [ 5] and humans [ 6] tend to involve the heart, liver, and nervous system, but some endocrine effects can occur. Saber Hussain, Syed F. Ali, in Handbook of Developmental Neurotoxicology, 1998. Given the overlapping clinical symptoms between manganism and PD, it is expected that DA neurotransmission is affected in both conditions. studies. Acute toxicity can cause frank psychosis, with visual and auditory hallucinations, euphoria, and compulsive behaviors. More recently, the role of astrocytes in manganese-mediated neurotoxicity has been investigated. Here, we show how a model organism for manganese oxidation is growth inhibited by nitrite, and that this inhibition is mitigated in the presence of manganese. The SOD activity is expressed as units/mg of protein; mean ± SEM for 6–8 animals per group. In a study by Brenneman et al. Most of the adverse events (65%) were moderate and 7% were severe. Contact with other Manganese biomineralization is a widespread process among bacteria and fungi. Studies with primary astrocyte cultures have revealed that they are a critical component in the defenses against manganese-induced neurotoxicity (Dobson et al., 2004). Karin Tuschl, ... Peter T. Clayton, in International Review of Neurobiology, 2013. to the accumulation of dark crystals of insoluble manganese dioxide in tissues within or alongside the veins (1, 3), and ... from manganese toxicity is displayed most notably in the cabbage family (Brassica spp.) Evidence obtained from laboratory animals indicates that exposure to high levels of Mn may adversely affect sperm quality (Elbetieha et al., 2001; Ponnapakkam et al., 2003a,b), cause decreased testicular weights (Laskey et al., 1982) and impair development of the male reproductive tract. (1994) in an experimental study performed on 6-month-old rats provided supporting evidence for the hypothesis that high levels of manganese exert neurotoxicity through oxidation. However, both the trivalent (MnIII) and divalent (MnII) forms have been demonstrated to be neurotoxic (Aschner and Aschner, 1991), but it is important to note that the oxidation of catechols is more efficient with Mn(III) than with Mn(II) or Mn(IV) (Achibald and Tyree, 1987). Emergency Number: 201-796-7100 ). Figure 12. In a similar study, neonatal rats exposed to Mn (0.31 mg Mn/kg/day for 60 days in water) suffered neuronal degeneration and increased brain monoamine oxidase on day 15 and 30 of the study, but did not show any clinical or behavioral signs of neurotoxicity (Chandra and Shukla, 1978). Advanced cases have shown fixed facial expression, emotional disturbances, spastic gait, and falling. The effect of MnCl2 on the activities of SOD and GPx and its effect on GSH content were evaluated in different regions of rat brain after administration at 2.5 or 5 mg MnCl2/kg. May Powdered manganese dioxide and chrome oxide are not toxic in skin absorption in the raw state, because the particles are A significant function of Mn is as a constituent of the antioxidant enzyme Mn-SOD, which catalyzes the dismutation of superoxide (O2–. Chim. For CHEMTREC assistance, call: 800-424-9300 Desole et al. This suggests that Mn may not effect cytosolic enzymes like Cu,Zn-SOD, but effects only Mn-SOD located in mitochondria. However, the disturbance is likely to occur at different points within the complex neuronal pathways in the basal ganglia (Roth, Li, Sridhar, & Khoshbouei, 2013).