Manganese Neurotoxicity and Oxidative Damage

Aschner, Michael

doi:10.1007/978-1-4899-0197-2_5

Cited by 35 publications

(16 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Section: Discussionmentioning

confidence: 97%

“…A recent study suggests that high levels of Mn in drinking water ([300 mg/l) are associated with reduced intellectual function (Wasserman et al 2006) and induced neurological disorders similar to Parkinson diseases (Aschner 1997;Lander et al 1999). Recent studies suggest that oxidative stress may play a key role in manganese-induced neurotoxicity (Aschner 1997;Galvani et al 1995). Therefore the brain is very susceptible to oxidative stress due to its high oxygen consumption, its high iron and lipid contents, especially polyunsaturated fatty acids (PUFA), and the low activity of antioxidant defenses, a fact that makes this tissue more vulnerable to increased levels of oxygen reactive species (Halliwell and Gutteridge 2007).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Silymarin, a natural antioxidant, protects cerebral cortex against manganese-induced neurotoxicity in adult rats

et al. 2010

View full text Add to dashboard Cite

Manganese (Mn) is an essential element for biological systems, nevertheless occupational exposure to high levels of Mn can lead to neurodegenerative disorders, characterized by serious oxidative and neurotoxic effects with similarities to Parkinson's disease. The aim of this study was to investigate the potential effects of silymarin (SIL), an antioxidant flavonoid, against manganese chloride induced neurotoxicity both in vivo (cerebral cortex of rats) and in vitro (Neuro2a cells). Twenty-eight male Wistar rats were randomly divided into four groups: the first group (C) received vehicle solution (i.p.) served as controls. The second group (Mn) received orally manganese chloride (20 mg/ml). The third group (Mn + SIL) received both Mn and SIL. The fourth group (SIL) received only SIL (100 mg/kg/day, i.p.). Animals exposed to Manganese chloride showed a significant increase in TBARS, NO, AOPP and PCO levels in cerebral cortex. These changes were accompanied by a decrease of enzymatic (SOD, CAT, GPx) and non-enzymatic (GSH, NpSH, Vit C) antioxidants. Co-administration of silymarin to Mn-treated rats significantly improved antioxidant enzyme activities and attenuated oxidative damages observed in brain tissue. The potential effect of SIL to prevent Mn induced neurotoxicity was also reflected by the microscopic study, indicative of its neuroprotective effects. We concluded that silymarin possesses neuroprotective potential, thus validating its use in alleviating manganese-induced neurodegenerative effects.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Silymarin, a natural antioxidant, protects cerebral cortex against manganese-induced neurotoxicity in adult rats

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Manganese can adopt different valences and is a powerful oxidant as the trivalent species (9). Together with dopamine, manganese can accelerate oxidation-reduction reactions, producing reactive oxidative molecules such as hydrogen peroxide and superoxide free radicals; this potentially explains the dopaminergic neurotoxicity seen in chronic manganese poisoning and the relief of symptoms by the administration of L-dopa in some patients (10)(11)(12)(13)(14). With relevance to the current case, derangements in dopamine metabolism have also been invoked as a mechanism underlying the syndrome of attention deficit hyperactivity disorder in some children (15,16).…”

Section: Discussionmentioning

confidence: 99%

A child with chronic manganese exposure from drinking water.

Woolf

Wright

Amarasiriwardena

et al. 2002

Environ Health Perspect

149

View full text Add to dashboard Cite

The patient's family bought a home in a suburb, but the proximity of the house to wetlands and its distance from the town water main prohibited connecting the house to town water. The family had a well drilled and they drank the well water for 5 years, despite the fact that the water was turbid, had a metallic taste, and left an orange-brown residue on clothes, dishes, and appliances. When the water was tested after 5 years of residential use, the manganese concentration was elevated (1.21 ppm; U.S. Environmental Protection Agency reference, < 0.05 ppm). The family's 10-year-old son had elevated manganese concentrations in whole blood, urine, and hair. The blood manganese level of his brother was normal, but his hair manganese level was elevated. The patient, the 10-year-old, was in the fifth grade and had no history of learning problems; however, teachers had noticed his inattentiveness and lack of focus in the classroom. Our results of cognitive testing were normal, but tests of memory revealed a markedly below-average performance: the patient's general memory index was at the 13th percentile, his verbal memory at the 19th percentile, his visual memory at the 14th percentile, and his learning index at the 19th percentile. The patient's free recall and cued recall tests were all 0.5-1.5 standard deviations (1 SD = 16th percentile) below normal. Psychometric testing scores showed normal IQ but unexpectedly poor verbal and visual memory. These findings are consistent with the known toxic effects of manganese, although a causal relationship cannot necessarily be inferred. Key words: ADHD, attention deficit hyperactivity disorder, manganese, manganese exposure, water, water pollution.

show abstract

“…90) Experimental observations suggest that secondary excitotoxic mechanisms play a crucial role in the development of manganese-induced neurodegeneration in the striatum. Centonze et al demonstrated that the abnormal excitation of striatal neurons during manganese intoxication may be due to hyperactivity of corticostriatal neurons.…”

Section: Manganese Movement and Action In The Synapsementioning

confidence: 99%

Analysis of Brain Function and Prevention of Brain Diseases: the Action of Trace Metals

Takeda

2004

JOURNAL OF HEALTH SCIENCE

View full text Add to dashboard Cite

Trace metals such as zinc, manganese, and iron are necessary for the growth and function of the brain. The transport of trace metals into the brain is strictly regulated by the brain barrier system, i.e., the blood-brain and blood-cerebrospinal fluid barriers. The alteration of homeostasis of trace metals in the brain is associated with brain diseases. Trace metals usually serve the function of metalloproteins in neurons and glial cells, while a portion of trace metals exists in the presynaptic vesicles and may be released with neurotransmitters into the synaptic cleft. Zinc and manganese influence the concentration of neurotransmitters in the synaptic cleft, probably via the action against neurotransmitter receptors and transporters and ion channels. Zinc may be an inhibitory neuromodulator of glutamate release in the hippocampus, while neuromodulation by manganese might have both functional and toxic aspects in the synapse. Dietary zinc deficiency affects zinc homeostasis in the brain, followed by an enhanced excitotoxicity of glutamate in the hippocampus. Transferrin may be involved in the physiologic transport of iron and manganese into the brain and their utilization there.

show abstract

Manganese Neurotoxicity and Oxidative Damage

Cited by 35 publications

References 75 publications

Silymarin, a natural antioxidant, protects cerebral cortex against manganese-induced neurotoxicity in adult rats

Silymarin, a natural antioxidant, protects cerebral cortex against manganese-induced neurotoxicity in adult rats

A child with chronic manganese exposure from drinking water.

Analysis of Brain Function and Prevention of Brain Diseases: the Action of Trace Metals

Contact Info

Product

Resources

About