Department of Zoology, University of Pune, Pune, India.
Islets. 2010 Jul-Aug;2(4):225-35. doi: 10.4161/isl.2.4.12219.
Pancreatic β-cells secrete insulin in response to changes in extracellular glucose concentration. Persistent hyperglycemia during diabetes exerts toxic effects on islets by creating redox imbalance arising from overproduction of reactive oxygen species (ROS). ROS accumulation disturbs the integrity and physiological function of cellular biomolecules impairing viability and functionality of cells. Susceptibility of an organ to oxidative stress (OS) is determined by its defense mechanism and ability to repair DNA damage caused by ROS. Weak defense status of islets along with its inefficiency to repair oxidative DNA damage as compared to other tissues renders it extraordinarily sensitive to OS. Realizing the vulnerability of islet cells to oxidative damage, several efforts to boost their defense mechanism in the form of oral administration of antioxidants and overexpression of genes responsible for antioxidant enzymes have proven successful. Recently accountability for this low antioxidant defense of islets have been given by correlating it with its metabolic evolution.
胰岛β细胞在细胞外葡萄糖浓度发生变化时会分泌胰岛素。糖尿病患者持续的高血糖会通过产生过多的活性氧（ROS）导致氧化还原失衡，对胰岛产生毒性作用。ROS 的积累扰乱了细胞生物分子的完整性和生理功能，损害了细胞的活力和功能。器官对氧化应激（OS）的敏感性取决于其防御机制和修复由 ROS 引起的 DNA 损伤的能力。与其他组织相比，胰岛的防御状态较弱，并且修复氧化 DNA 损伤的效率较低，这使其对 OS 非常敏感。鉴于胰岛细胞对氧化损伤的脆弱性，人们通过口服抗氧化剂和过表达负责抗氧化酶的基因来增强其防御机制的几种努力已经取得了成功。最近，人们通过将胰岛的低抗氧化防御能力与其代谢进化相关联，为其提供了相应的解释。
