Fish Oil and Antipsychotic Drug Risperidone Modulate Oxidative Stress in PC12 Cell Membranes Through Regulation of Cytosolic Calcium Ion Release and Antioxidant System

Abstract

Oxidative stress is a critical route of damage in various psychological disorders such as schizophrenia, although fish oil and risperidone (RISP) induce antioxidant effects in the human body. However, the mechanisms behind these effects remain elusive. We investigated the effects of fish oil and RISP in the PC12 cell line by evaluating Ca(2+) mobilization, lipid peroxidation (LP) and antioxidant levels. PC12 cells were divided into eight flasks: control, fish oil, RISP, H(2)O(2), fish oil + H(2)O(2), RISP + H(2)O(2), fish oil + RISP and fish oil + RISP + H(2)O(2). Cells were incubated with fish oil and RISP for 24 and 48 h, respectively. Then, cells were exposed to H(2)O(2) for 15 min before analysis. Ca(2+) release and LP levels were higher in the H(2)O(2) group than in the control, RISP and fish oil groups, although their levels were decreased by incubation of cells in fish oil and RISP. Glutathione peroxidase activity, reduced glutathione and vitamin C levels in the cells were lower in the H(2)O(2) group than in the control, RISP and fish oil groups, although levels were higher in cells incubated with fish oil and RISP than in those in the H(2)O(2) groups. In conclusion, these results indicate that RISP and fish oil induced protective effects on oxidative stress in PC12 cells by modulating cytosolic Ca(2+) release and antioxidant levels.

Effects of Selenium and Topiramate on Cytosolic Ca2+ Influx and Oxidative Stress in Neuronal PC12 Cells

“…Before treatment, PC-12 cells were placed in poly-D-lysine coated cell culture flask at a density of 2 9 10 5 per well and were allowed to attach for 24 h in RPMI 1640 medium supplemented with 10 % donor horse serum, and a mixture of 1 % of penicillin/streptomycin/L-glutamine. Cells were incubated at Neurochem Res (2013) 38:90-97 91 37°C in humid, 5 % CO 2 and 95 % air environment [16]. Differentiation of the cells was induced by addition of nerve growth factor (NGF) to the cultures (50 ng/ml) for 2 days.…”

“…PC12 cells have been widely used in studies of oxidative stress-induced protection models [16]. Since it has not yet been clarified the modulator effects of selenium and TPM on the cellular survival and death in molecular pathways, we hence focused on the dual effect of selenium and TPM in undifferentiated PC12 cell lines by checking its role on lipid peroxidation and antioxidant levels and Ca 2?…”

Hydrogen peroxide attenuates refilling of intracellular calcium store in mouse pancreatic acinar cells

“…Although cytosolic H 2 O 2 concentrations produced by oxidative stress in pancreatic acinar cells is not known, only small proportion of cells (34%) were response to 100 µM of H 2 O 2 and most cells (97%) were response to 300 µM of H 2 O 2 in the present study. In general, H 2 O 2 at concentrations from 10 µM to 1 mM caused intracellular Ca 2+ accumulation in various cell types [1011,12,13,14,15,16,17]. These results suggest that excess generation of oxidants in pathologic conditions could disturb Ca 2+ homeostasis mediated by sulfhydryl group oxidation in pancreatic acinar cells.…”

“…Although oxidant-induced intracellular Ca 2+ overload has been revealed in various cell types, the underlying mechanisms of Ca 2+ mobilization and elimination are complicated [1011,12,13,14,15,16,1718]. It has been known that the involvement of oxidants in Ca 2+ homeostasis is mediated by the modification of disulfide bonds between cysteine residues of Ca 2+ regulating proteins including SERCA, PMCA and Na + /Ca 2+ exchanger (NCX) [3132].…”

“…However, the mechanism of H 2 O 2 -induced Ca 2+ accumulation has known to be complicated due to cell-to-cell difference in expression and participation of Ca 2+ modulating transporters. It has been reported that H 2 O 2 can enhance Ca 2+ release from intracellular store [101112], stimulate Ca 2+ entry from extracellular medium [13141516], and attenuate Ca 2+ extrusion by plasma membrane Ca 2+ ATPase (PMCA) or sarco/endoplasmic reticulum Ca 2+ ATPase (SERCA) inactivation [1718] in various cell types.…”