義守大學（後中醫）
113年
英文
第 50 題
📖 題組：
Respiratory diseases cover a broad spectrum, from upper respiratory tract infections to serious conditions like chronic obstructive pulmonary disease (COPD), asthma, pulmonary fibrosis (PF), acute respiratory distress syndrome (ARDS), acute lung injury (ALI), lung ischemia–reperfusion injury (LIRI), pulmonary hypertension (PH), and lung cancer. These conditions, characterized by structural changes in airway and lung tissues and reduced respiratory function, pose significant health and economic burdens worldwide. Notably, COVID-19 caused 18 million deaths between 2020 and 2021, further emphasizing the global challenge of respiratory diseases. COPD is the third leading cause of death globally, while ARDS and ALI account for no less than 4% of U.S. hospitalizations annually. Lung cancer, leading in cancer-related deaths, saw 2.24 million new cases and 1.8 million fatalities in 2020, as reported by the International Agency for Research on Cancer. Risk factors include smoking, air pollution, infections, and obesity. Despite the availability of treatments like antibiotics and lung transplants, their side effects have prompted the search for innovative therapeutic approaches. First introduced by Dixon et al. in 2012, ferroptosis is a form of programmed cell death (PCD), a term distinct from other modes of cell death such as necrosis, apoptosis, autophagy, necroptosis, and pyroptosis, which is essential for maintaining homeostatic balance. Morphologically, ferroptosis features mitochondrial shrinkage, denser membranes, and reduced mitochondrial cristae, with an intact cell membrane and normal-sized nucleus without chromatin condensation. Biochemically, ferroptosis is triggered by the depletion of intracellular glutathione (GSH) and a decrease in the activity of glutathione peroxidase 4 (GPX4). This imbalance leads to lipid peroxidation, further exacerbated by $Fe^{2+}$ through the Fenton reaction, generating a high concentration of reactive oxygen species (ROS).
Respiratory diseases cover a broad spectrum, from upper respiratory tract infections to serious conditions like chronic obstructive pulmonary disease (COPD), asthma, pulmonary fibrosis (PF), acute respiratory distress syndrome (ARDS), acute lung injury (ALI), lung ischemia–reperfusion injury (LIRI), pulmonary hypertension (PH), and lung cancer. These conditions, characterized by structural changes in airway and lung tissues and reduced respiratory function, pose significant health and economic burdens worldwide. Notably, COVID-19 caused 18 million deaths between 2020 and 2021, further emphasizing the global challenge of respiratory diseases. COPD is the third leading cause of death globally, while ARDS and ALI account for no less than 4% of U.S. hospitalizations annually. Lung cancer, leading in cancer-related deaths, saw 2.24 million new cases and 1.8 million fatalities in 2020, as reported by the International Agency for Research on Cancer. Risk factors include smoking, air pollution, infections, and obesity. Despite the availability of treatments like antibiotics and lung transplants, their side effects have prompted the search for innovative therapeutic approaches. First introduced by Dixon et al. in 2012, ferroptosis is a form of programmed cell death (PCD), a term distinct from other modes of cell death such as necrosis, apoptosis, autophagy, necroptosis, and pyroptosis, which is essential for maintaining homeostatic balance. Morphologically, ferroptosis features mitochondrial shrinkage, denser membranes, and reduced mitochondrial cristae, with an intact cell membrane and normal-sized nucleus without chromatin condensation. Biochemically, ferroptosis is triggered by the depletion of intracellular glutathione (GSH) and a decrease in the activity of glutathione peroxidase 4 (GPX4). This imbalance leads to lipid peroxidation, further exacerbated by $Fe^{2+}$ through the Fenton reaction, generating a high concentration of reactive oxygen species (ROS).
What distinguishes ferroptosis from other programmed cell death (PCD) forms?
- A It is the only form of PCD without an impact on the mitochondria.
- B It is a reversible process that does not lead to cell death.
- C It results exclusively from external physical trauma.
- D It features mitochondrial shrinkage and is triggered by the depletion of intracellular glutathione (GSH).
思路引導 VIP
若要在一篇介紹多種生物機制的文章中，找出某種特定現象與眾不同的「專屬識別證」，你會建議讀者特別留意文中哪些關於「微觀形狀改變」以及「化學物質含量增減」的具體描述呢？
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AI 詳解
AI 專屬家教
恭喜你準確地掌握了文章的細節！這題要求考生從稍具難度的學術文本中，精確定位特定科學術語的定義特徵。你能從長篇描述中辨識出「鐵死亡」（ferroptosis）的關鍵機制，展現了非常優秀的閱讀理解與資訊檢索能力。
鐵死亡的特徵辨析
根據文章第三段的說明，鐵死亡與其他程序性細胞死亡（PCD）的主要區別在於其獨特的形態與生化路徑。在形態學（Morphologically）上，它表現為線粒體萎縮（mitochondrial shrinkage）與膜密度增加；而在生化面（Biochemically），則是由於細胞內穀胱甘肽（$GSH$）的耗竭，導致穀胱甘肽過氧化物酶 4（$GPX4$）活性下降，進而引發脂質過氧化反應。選項 (D) 正確地結合了這兩大核心觀察點。
▼ 還有更多解析內容
鐵死亡的特徵與機制
💡 鐵死亡是以脂質過氧化與線粒體萎縮為特徵的細胞死亡方式。
🔗 鐵死亡生化機制連鎖反應
- 1 誘發因子 — GSH 耗竭或 GPX4 酵素活性降低
- 2 生化反應 — 鐵離子催化 Fenton 反應產生大量 ROS
- 3 關鍵損害 — 脂質過氧化物大量堆積破壞膜結構
- 4 形態特徵 — 線粒體萎縮、膜密度增高，細胞死亡
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🔄 延伸學習：延伸學習：了解鐵死亡在癌症化療與呼吸道疾病（如 COPD）中的病理作用。
