Brain Lipid Peroxidation and Changes of Trace Metals in Rats Following Chronic Manganese Chloride Exposure

Chen, Min-Tzu; Yiin, Shuenn-Jiun; Sheu, Jenn-Yuan; Huang, Yeou‐Lih

doi:10.1080/15287390252800882

Cited by 14 publications

(8 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PC12 cells treated for 48 h also presented a reduced content of Chol and of eicosapentaenoic acid (C20:5) and docosahexaenoic acid (C22:6), which are n-3 PUFA involved in important membrane-mediated processes [40]. The decrease in n-3 PUFA could be due to an increase in lipid peroxidation, since it has been reported that Mn-induced apoptosis is associated with oxidative stress [41][42][43]. Interestingly, the overall modifications of the lipid content results in an increase of phospholipids/ Chol and in a decrease of PE/PC ratios, which indicated an increase in membrane fluidity.…”

Section: Discussionmentioning

confidence: 95%

Changes in Lipid Composition During Manganese-Induced Apoptosis in PC12 Cells

et al. 2015

View full text Add to dashboard Cite

Lipid composition of membranes is fundamental to modulate signaling pathways relying on lipid metabolites and/or membrane proteins, thus resulting in the regulation of important cell processes such as apoptosis. In this case, membrane remodeling is an early event important for the activation of signaling leading to cell death and removal of apoptotic cells. In the present study, we analyzed phospholipid, cholesterol and fatty acid content during apoptosis induced by manganese in PC12 cells. Lipid analysis of whole cells and detergent-resistant membranes was carried out by HPLC/GC. Results showed that apoptosis is associated with changes in lipid composition detectable in whole cell extracts, namely cholesterol, phosphatidylserine and phosphatidylethanolamine decreases. Noteworthy, phosphatidylserine level reduction was detectable before to the detection of apoptosis, in correlation with our previous study carried out by radioactive labelling. By contrast, phosphatidylserine and phosphatidylethanolamine changes were not detected in detergent resistant membranes, which instead showed an altered composition in phosphatidylinositol, phosphatidylcholine and sphingomyelin in apoptotic cells.

show abstract

Section: Discussionmentioning

confidence: 95%

Changes in Lipid Composition During Manganese-Induced Apoptosis in PC12 Cells

et al. 2015

View full text Add to dashboard Cite

show abstract

“…An elevated level of MDA reflects, to a certain degree, tissue injury resulting from oxidative damage. Results from animal studies showed an alteration of MDA level in animals exposed to Mn (Chen et al, 2002). Misiewicz and colleagues (1999) also demonstrated an increased serum concentration of MDA in workers engaged in the production of Fe-Mn alloys.…”

Section: Biomarkers Of Mn Toxicitiesmentioning

confidence: 99%

Biomarkers of manganese intoxication

et al. 2011

View full text Add to dashboard Cite

Manganese (Mn), upon absorption, is primarily sequestered in tissue and intracellular compartments. For this reason, blood Mn concentration does not always accurately reflect Mn concentration in the targeted tissue, particularly in the brain. The discrepancy between Mn concentrations in tissue or intracellular components means that blood Mn is a poor biomarker of Mn exposure or toxicity under many conditions and that other biomarkers must be established. For group comparisons of active workers, blood Mn has some utility for distinguishing exposed from unexposed subjects, although the large variability in mean values renders it insensitive for discriminating one individual from the rest of the study population. Mn exposure is known to alter iron (Fe) homeostasis. The Mn/Fe ratio (MIR) in plasma or erythrocytes reflects not only steadystate concentrations of Mn or Fe in tested individuals, but also a biological response (altered Fe homeostasis) to Mn exposure. Recent human studies support the potential value for using MIR to distinguish individuals with Mn exposure. Additionally, magnetic resonance imaging (MRI), in combination with noninvasive assessment of γ-aminobutyric acid (GABA) by magnetic resonance spectroscopy (MRS), provides convincing evidence of Mn exposure, even without clinical symptoms of Mn intoxication. For subjects with long-term, low-dose Mn exposure or for those exposed in the past but not the present, neither blood Mn nor MRI provides a confident distinction for Mn exposure or intoxication. While plasma or erythrocyte MIR is more likely a sensitive measure, the cut-off values for MIR among the general population need to be further tested and established. Considering the large accumulation of Mn in bone, developing an X-ray fluorescence spectroscopy or neutron-based spectroscopy method may create yet another novel non-invasive tool for assessing Mn exposure and toxicity.

show abstract

“…Some researchers have reported an alteration of MDA level in animals exposed to manganese. 26 Misiewicz and his colleagues 27 also demonstrate an increased serum concentration of MDA in workers engaged in the production of ironmanganese alloys. Therefore, the levels of either SOD or MDA, or both, in the systemic circulation may serve as the useful biomarker(s) for oxidative status after long-term, lowlevel exposure to the welding fume among career welders.…”

mentioning

confidence: 97%

“…Because in vivo exposure to manganese has been shown to induce the oxidative stress, 26,27 the activities of SOD and levels of MDA were assayed to test the hypothesis that altered SOD and/or MDA among welders may be used as the biomarker(s) for manganese exposure in humans. Table 4 summarizes the comparisons made between welders and control subjects.…”

Section: Systemic Status Of Oxidative Stressmentioning

confidence: 99%

Occupational Exposure to Welding Fume among Welders: Alterations of Manganese, Iron, Zinc, Copper, and Lead in Body Fluids and the Oxidative Stress Status

Zhang

et al. 2004

Journal of Occupational and Environmental Medicine

147

View full text Add to dashboard Cite

Welders in this study were selected from a vehicle manufacturer; control subjects were from a nearby food factory. Airborne manganese levels in the breathing zones of welders and controls were 1.45 ± SD1.08 mg/m 3 and 0.11 ± 0.07 μg/m 3 , respectively. Serum levels of manganese and iron in welders were 4.3-fold and 1.9-fold, respectively, higher than those of controls. Blood lead concentrations in welders increased 2.5-fold, whereas serum zinc levels decreased 1.2-fold, in comparison with controls. Linear regression revealed the lack of associations between blood levels of five metals and welder's age. Furthermore, welders had erythrocytic superoxide dismutase activity and serum malondialdehyde levels 24% less and 78% higher, respectively, than those of controls. These findings suggest that occupational exposure to welding fumes among welders disturbs the homeostasis of trace elements in systemic circulation and induces oxidative stress.The welding fume generated during the welding process possesses at least 13 metals, including manganese (Mn), beryllium (Be), cadmium (Cd), chromium (Cr), cobalt (Co), copper (Cu), iron (Fe), lead (Pb), mercury (Hg), molybdenum (Mo), nickel (Ni), zinc (Zn), antimony (Sb), and vanadium (V). 1 Welders are known to be at risk, particularly for chronic exposure to airborne manganese, which is one of the major coating materials in welding products (eg, bars and wires). [2][3][4][5][6] A recent study even suggests that exposure to manganese during welding may be a risk factor for the etiology of Parkinson's disease among the career welders. 7 Although limited studies have documented airborne manganese levels during welding, the question as to how low-level, long-term exposure to manganese or welding fume may affect blood levels of trace metals is unanswered. However, altered systemic homeostasis of iron and manganese is known to be associated with neurodegenerative disorders. 8 Manganese-induced neurological lesions are reportedly located in the globus pallidus and striatum of the basal ganglia. The pallidus and striatum display a marked decrease in myelinated nerve fibers, accompanied by depletion of striatal dopamine. [11][12][13][14] The mechanism whereby manganese induces neurodegenerative damage remains elusive. Nonetheless, several recent reports have suggested that manganese neurotoxicity may be associated with its interaction with other essential trace elements, including iron, 10,13,15,16 zinc, 17 copper, 17 and aluminum. 13,15,18 Particularly regarding manganese-induced neurotoxicity, studies have shown that chronic exposure to manganese appears to be associated with altered iron concentrations in blood as well as in the cerebrospinal fluid, presumably the result of Mn-Fe interaction at certain [Fe-S]-containing proteins, which regulate the homeostasis of iron. 10,16,[19][20][21] The excess accumulation of iron in neurons may consequently produce cellular oxidative stress, leading to neuronal damage.Superoxide dismutase (SOD), a cytoplasmic enzyme, catalyzes the react...

show abstract

Brain Lipid Peroxidation and Changes of Trace Metals in Rats Following Chronic Manganese Chloride Exposure

Cited by 14 publications

References 37 publications

Changes in Lipid Composition During Manganese-Induced Apoptosis in PC12 Cells

Changes in Lipid Composition During Manganese-Induced Apoptosis in PC12 Cells

Biomarkers of manganese intoxication

Occupational Exposure to Welding Fume among Welders: Alterations of Manganese, Iron, Zinc, Copper, and Lead in Body Fluids and the Oxidative Stress Status

Contact Info

Product

Resources

About