Nrf2 affects DNA damage repair and cell apoptosis through regulating HR and the intrinsic Caspase-dependent apoptosis pathway in TK6 cells exposed to hydroquinone.
Lin ChenPu GuoLu ZhaiLingxue YuDelong ZhuXiaoyi HuZhuanzhuan LiYuting ChenQian SunLei SunHao LuoHuanwen TangPublished in: Toxicology in vitro : an international journal published in association with BIBRA (2024)
Hydroquinone (HQ) is one of benzene metabolites that can cause oxidative stress damage and Homologous recombination repair (HR). A good deal of reactive oxygen species (ROS) generated by oxidative stress can trigger apoptotic signaling pathways. The nuclear factor erythroid 2-related factor 2 (Nrf2) can regulate the cell response to oxidative stress damage. The aim of this study was to explore whether Nrf2 participate in HQ-induced apoptosis and its mechanism. The findings displayed that HQ triggered HR, promoted Nrf2 transfer into the cell nucleus and induced cell apoptosis, while Nrf2 deficient elevated cell apoptosis, attenuated the expression of PARP1 and RAD51. We also observed that Nrf2 deficient triggered Caspase-9. Thus, we speculated that Nrf2 might participate in HQ-induced cell apoptosis through Caspase-9 dependent pathways. Meanwhile, Nrf2 participated in HQ-induced DNA damage repair by regulating the level of PARP1 and RAD51.
Keyphrases
- oxidative stress
- induced apoptosis
- dna damage
- diabetic rats
- dna repair
- ischemia reperfusion injury
- cell proliferation
- endoplasmic reticulum stress
- nuclear factor
- reactive oxygen species
- cell death
- signaling pathway
- single cell
- high glucose
- toll like receptor
- heat shock
- inflammatory response
- poor prognosis
- stem cells
- drug induced
- mesenchymal stem cells
- endothelial cells
- immune response