AhR agonism or antagonism does not cause cytotoxicity in hNPCs and mNPCs.
We verified this using hNPCs derived from a second individual (data not shown).
In contrast to the hNPCs, we observed significant inhibition of mNPC proliferation after 7 days of exposure to 1 [micro]M MNF.
This was verified using hNPCs from a second individual (data not shown).
As shown in Figure 2, Annexin V-PI staining assays detected significantly increased Annexin V-positive apoptotic cells in 50 nM MeHg-treated hNPCs than the control group (0 nM: 3.
In this study, the effect of MeHg on the generation of ROS in hNPCs was measured by the DCFH-DA assay (Figure 3(a)).
MeHg Alters Mitochondrial mRNA Transcripts and Mitochondrial Functions in hNPCs.
Moreover, to examine the underlying changes of mitochondrial function induced by MeHg, we then assessed mitochondrial membrane potential ([DELTA][psi]m) and ATP cellular content as indicators of mitochondrial function in hNPCs.
In contrast, BDE-47 and BDE-99 increased nestin expression 4- and 5-fold, showing that PBDEs delay differentiation of hNPCs (Figure 3B).
In contrast, NH-3 inhibited migration of hNPCs to 735.
Exposure of hNPCs to 1 [micro]M (14) C-BDE-47 for 7 days resulted in a cellular concentration of 61.
To shed light onto the effects caused by PBDE exposure in human developing brain cells, we studied their effects on the development of hNPCs in vitro.