心磷脂
线粒体
脂质过氧化
生产过剩
化学
电子传输链
活性氧
细胞生物学
生物化学
生物
氧化应激
膜
基因
磷脂
作者
Itzel Reyna-Bolaños,Eduardo Solís-García,Manuel Alejandro Vargas-Vargas,Donovan J. Peña‐Montes,Alfredo Saavedra‐Molina,Christian Cortés‐Rojo,Elizabeth Calderón‐Cortés
标识
DOI:10.3390/ijms252011104
摘要
Increased intramitochondrial free iron is a key feature of various liver diseases, leading to oxidative stress, mitochondrial dysfunction, and liver damage. Polydatin is a polyphenol with a hepatoprotective effect, which has been attributed to its ability to enhance mitochondrial oxidative metabolism and antioxidant defenses, thereby inhibiting reactive oxygen species (ROS) dependent cellular damage processes and liver diseases. However, it has not been explored whether polydatin is able to exert its effects by protecting the phospholipid cardiolipin against damage from excess iron. Cardiolipin maintains the integrity and function of electron transport chain (ETC) complexes and keeps cytochrome c bound to mitochondria, avoiding uncontrolled apoptosis. Therefore, the effect of polydatin on oxidative lipid damage, ETC activity, cytochrome levels, and ROS production was explored in iron-exposed rat liver mitochondria. Fe2+ increased lipid peroxidation, decreased cardiolipin and cytochromes c + c1 and aa3 levels, inhibited ETC complex activities, and dramatically increased ROS production. Preincubation with polydatin prevented all these effects to a variable degree. These results suggest that the hepatoprotective mechanism of polydatin involves the attenuation of free radical production by iron, which enhances cardiolipin levels by counteracting membrane lipid peroxidation. This prevents the loss of cytochromes, improves ETC function, and decreases mitochondrial ROS production.
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