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东北贯众素/标准品/对照品
兽药残留酶免实验室建设方案
API Listeria
细胞功能检测(细胞凋
EpiMethy DNA甲基化检
心血管类疾病模型
Annexin V-EGFP/PI双
CVTK细胞增殖与毒性检
免疫印迹化学发光试剂
Tofacitinib citrate 
细胞周期与凋亡检测试D6883-50MG
国内现货
Oxidative stress is implicated in the pathogenesis of lipotoxicity in both animal and human studies. Chronic oxidative stress is linked to insulin resistance in multiple tissues. Oxidative stress is mediated, in part, by reactive oxygen species produced by multiple cellular processes and controlled by cellular antioxidant mechanisms such as enzymatic scavengers or antioxidant modulators. When ROS production exceeds the cellular antioxidant capacity, oxidative damage to cellular components such as proteins, lipids, and DNA occurs. Multiple pathways can contribute to cellular ROS formation, including the mitochondrial electron transport chain (ETC), inflammatory signaling, and endoplasmic reticulum stress.
The ETC is the major source of endogenous superoxide production in the cell. As electrons pass through the ETC, a small fraction escape and prematurely react with molecular oxygen resulting in the production of superoxide. An excess of nutrients will theoretically increase electron flux through the ETC with a resulting increase in the production of superoxide. Excessive ROS production may induce insulin resistance by the activation of stress-activated signaling cascades or by causing damage to mitochondrial proteins and DNA.
