Some POPs alter cells via a non-ROS mechanisms ...
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2,3,7,8-tetrachlorobenzo-p-dioxin inhibits proliferation of SK-N-SH
human neuronal cells through decreased production of reactive oxygen
species.
Oxidative stress has been known to be involved in the mechanism of
toxic effects of various agents on many cellular systems. In this
study we investigated the role of reactive oxygen species (ROS) in
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced neuronal cell
toxicity using SK-N-SH human neuroblastoma cells. TCDD inhibited
proliferation of the cells in a dose-dependent manner, which was
revealed by MTT staining, counting of cells stained with trypan blue
and [3H]thymidine uptake assay. TCDD also suppressed the basal
generation of ROS in a time- and concentration-dependent manner
assessed by 2',7'-dichlorofluorescein fluorescence. In addition, TCDD
induced a dose-dependent inhibition of lipid peroxidation, a biomarker
of oxidative stress, whereas it significantly increased the level of
glutathione (GSH), an intracellular free radical scavenger in the
cells. Moreover, TCDD altered the activities of major antioxidant
enzymes; increase in superoxide dismutase (SOD) and catalase, but
decrease in glutathione peroxidase (GSH-Px) and glutathione reductase
(GSH-Red). Pretreatment with L-buthionine-S,R-sulfoximine (BSO, 50
microM), an inhibitor of GSH synthesis, significantly prevented the
TCDD-induced reduction in lipid peroxidation and cell proliferation.
Interestingly, exogenous application of an oxidant, H2O2 (50 microM)
markedly restored the inhibited cell proliferation induced by TCDD.
Taken together, these results suggest that alteration of cellular
redox balance may mediate the TCDD-induced inhibition of proliferation
in human neuronal cells. PMID: 12607819