A transcriptionally induced antioxidant program is elicited in thyroid cells after exposure to hydrogen peroxide
Ontology highlight
ABSTRACT: Radiation is an established cause of thyroid cancer and growing evidence supports a role for H2O2 in spontaneous thyroid carcinogenesis. Little is known about the molecular programs activated by these agents in thyroid cells. We profiled the DNA damage response and cell death induced by M-NM-3-radiation (0.1M-bM-^@M-^S5Gy) and H2O2 (0.0025M-bM-^@M-^S0.3mM) in primary human thyroid cells and T-cells. While the two cell types had more comparable radiation responses, 3- to 10-fold more H2O2 was needed to induce detectable DNA damage in thyrocytes. At H2O2 and radiation doses incurring double-strand breaks (DSB), cell death occurred after 24hrs in T-cells, but not in thyrocytes. We next prepared thyroid and T-cells primary cultures from 8 donors operated for non-cancerous pathologies and profi
ORGANISM(S): Homo sapiens
SUBMITTER: Maxime Tarabichi
PROVIDER: E-GEOD-39156 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
ACCESS DATA