Effects of Manganese on Oxidative Stress in CATH.a Cells

Worley, Cynthia G; Bombick, David W.; Allen, Jeffrey W.; Suber, Robert L.; Aschner, Michael

doi:10.1016/s0161-813x(02)00028-1

Cited by 22 publications

(15 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mn content showed contradictory effects; we observed both negative and positive correlations between this mineral and the antimutagenic activity of grape juices. Mn can act as both pro-and antioxidant, and the oxidative-stress-related effects of Mn are dependent not only on the intracellular concentrations of the metal but also on the exposure duration, secondary oxidative challenges, and overall oxidant-buffering ability of the cells (Worley et al, 2002).…”

Section: Resultsmentioning

confidence: 99%

Mineral content is related to antioxidant and antimutagenic properties of grape juice

Dani¹,

Oliboni²,

Prá³

et al. 2012

Genet. Mol. Res.

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

Mineral content is related to antioxidant and antimutagenic properties of grape juice

Dani¹,

Oliboni²,

Prá³

et al. 2012

Genet. Mol. Res.

View full text Add to dashboard Cite

“…Moreover, allopurinol treatment protected against Mn induced oxidative stress in striatum in vivo [11]. Contrasting evidence also exists showing that Mn did not generate ROS in catecholaminergic CATH.a cells though prior administration of Mn increased H 2 O 2 -generated ROS more than H 2 O 2 alone [12] and also Mn did not produce oxidative stress in developing brains of neonatal rats [13].…”

Section: Introductionmentioning

confidence: 97%

Manganese-Induced Neurotoxicity is Differentially Enhanced by Glutathione Depletion in Astrocytoma and Neuroblastoma Cells

et al. 2006

View full text Add to dashboard Cite

Manganese (Mn) is neurotoxic: the underlying mechanisms have not been fully elucidated. L: -Buthionine-(S,R)-sulfoximine (BSO) is an irreversible inhibitor of gamma-glutamylcysteine synthetase, an important enzyme in glutathione (GSH) synthesis. To test the hypothesis that BSO modulates Mn toxicity, we investigated the effects of treatment of U-87 or SK-N-SH cells with MnCl(2), BSO, or MnCl(2) plus BSO. We monitored cell viability using MTT assay, staining with HO-33342 to assess live and/or apoptotic cells, and staining with propidium iodide (PI) to assess necrotic cells; we also measured cellular glutathione. Our results indicate decreased viability in both cell types when treated with MnCl(2) or BSO: Mn was more toxic to SK-N-SH cells, whereas BSO was more toxic to U-87 cells. Because BSO treatment accentuated Mn toxicity in both cell lines, GSH may act to combat Mn toxicity. Thus, further investigation in oxidative stress mediated by glutathione depletion will unravel new Mn toxicity mechanism(s).

show abstract

“…One mechanism proposed for manganese neurotoxicity is oxidative stress (19)(20)(21). In support of this mechanism, pathological concentration of manganese have been shown to produce reactive oxygen species (ROS) in vivo (22), in isolated rat brain mitochondria (23) and in cultured astrocytes (24).…”

Section: Introductionmentioning

confidence: 98%

Combined Effects of Ammonia and Manganese on Astrocytes in Culture

et al. 2004

View full text Add to dashboard Cite

Ammonia has been strongly implicated in the pathogenesis of hepatic encephalopathy (HE), and astrocytes appear to be the primary target of ammonia neurotoxicity. Recent work has shown that manganese also plays a role in the pathogenesis of HE and causes astrocyte morphologic and functional changes similar to ammonia. We therefore investigated whether a combination of these compounds could produce additive/synergistic effects. Cultured astrocytes treated with 5 mM ammonia (NH4Cl) along with 100 microM manganese acetate (MnAc) for 3 h showed a 55-65% increase in free radical production over ammonia or manganese alone (P < 0.05). There was also a 50% decrease in the mitochondrial membrane potential (beta psi(m)) at 24 h following treatment with NH4Cl (5 mM) plus MnAc (50 microM) (P < 0.05), as compared to ammonia or manganese alone. Astrocytes treated with ammonia or manganese alone for 24 h showed no cell death, as determined by LDH release and light microscopic examination. However, cultures treated with ammonia plus manganese showed 80-90% necrotic cell death as estimated by light microscopy and 59% cell death as determined by LDH release. LDH release by ammonia plus manganese was blocked by the antioxidant superoxide dismutase (25 units/ml) as well as by the nitric oxide synthase inhibitor N(omega)-nitro-L-argininemethyl ester (500 microM). In conclusion, ammonia plus manganese exert additive/synergetic effects on the induction free radicals, mitochondrial inner membrane depolarization and cellular integrity, which may contribute to the tissue injury associated with chronic forms of HE.

show abstract

Effects of Manganese on Oxidative Stress in CATH.a Cells

Cited by 22 publications

References 15 publications

Mineral content is related to antioxidant and antimutagenic properties of grape juice

Mineral content is related to antioxidant and antimutagenic properties of grape juice

Manganese-Induced Neurotoxicity is Differentially Enhanced by Glutathione Depletion in Astrocytoma and Neuroblastoma Cells

Combined Effects of Ammonia and Manganese on Astrocytes in Culture

Contact Info

Product

Resources

About