Low Doses of Arsenic in a Mouse Model of Human Exposure and in Neuronal Culture Lead to S-Nitrosylation of Synaptic Proteins and Apoptosis via Nitric Oxide.
Haitham AmalGuanyu GongHongmei YangBrian A JoughinXin WangCharles G KnutsonMaryam KartawyIgor KhaliulinJohn S WishnokSteven R TannenbaumPublished in: International journal of molecular sciences (2020)
This work develops a mechanistic understanding of the role of NO in arsenic-mediated toxicity in the brain, incorporating Ca2+ release and S-nitrosylation as important modifiers of neuronal protein function.
Keyphrases
- nitric oxide
- mouse model
- cerebral ischemia
- drinking water
- oxidative stress
- endothelial cells
- heavy metals
- endoplasmic reticulum stress
- white matter
- resting state
- induced pluripotent stem cells
- cell cycle arrest
- subarachnoid hemorrhage
- nitric oxide synthase
- cell death
- pluripotent stem cells
- hydrogen peroxide
- protein protein
- binding protein
- brain injury
- amino acid
- functional connectivity
- risk assessment
- pi k akt