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The effect of manganese exposure on endogenous markers of oxidative stress in astrocytes
Author(s) -
Fordahl Steve,
Anderson Joel,
Milatovic Dejan,
Aschner Michael,
Erikson Keith
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.729.1
Subject(s) - oxidative stress , glutathione , antioxidant , chemistry , lipid peroxidation , neuroprotection , endogeny , pharmacology , medicine , biochemistry , endocrinology , enzyme
Manganese (Mn) is an essential trace element; however, accumulation of Mn in the brain can propagate cellular damage leading to neuronal dysfunction and symptoms analogous to neurodegenerative disorders (i.e. Parkinson's disease). Previously our lab has shown that iron deficiency significantly increases Mn accumulation decreasing glutathione (GSH) functionality. The resulting oxidative damage may alter the neuronal environment leading to dysfunction. Our goal is twofold; to characterize how Mn accumulation in astrocytes leads to lipid peroxidation (LP), and to test the efficacy of á‐tocopherol or N‐acetyl cysteine therapy in attenuating the production of F2Isoprostanes (F2Isop), a marker of LP. Primary rat astrocytes were treated with 100 or 300 ìM Mn with or without antioxidant therapy. GSH, F2Isop, and Mn levels were measured to assess overall oxidative stress. Mn exposure significantly increased GSH levels in the absence of antioxidant treatment (p<0.005), though no difference in GSH was seen in any antioxidant treatment compared to control. Significant increases in F2Isop (p<0.05) were present in Mn treated cells and attenuated by antioxidant pretreatment. These data imply that Mn induced LP is due to alterations in the GSH protective system, but may be mitigated by antioxidant therapy. Funded by NINDS 1R15NS061309‐01