Article
Cell Biology
Catherine A. Bellissimo, Luca J. Delfinis, Meghan C. Hughes, Patrick C. Turnbull, Shivam Gandhi, Sara N. DiBenedetto, Fasih A. Rahman, Peyman Tadi, Christina A. Amaral, Ali Dehghani, James N. Cobley, Joe Quadrilatero, Uwe Schlattner, Christopher G. R. Perry
Summary: This study aimed to determine whether the prospective mitochondrial-enhancing compound Olesoxime can prevent early-stage mitochondrial stress in limb and respiratory muscle from D2.mdx mice. Results showed that Olesoxime selectively preserved or maintained muscle sensitivity to creatine, reduced creatine kinase release, and improved some indices of muscle quality.
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
(2023)
Article
Environmental Sciences
Kuiyang Zuo, Qi Xu, Yujie Wang, Yutong Sui, Ye Niu, Zinan Liu, Mingsheng Liu, Xinpeng Liu, Dan Liu, Wei Sun, Ziyu Wang, Xiaomei Liu, Jinyu Liu
Summary: Methylmercury (MeHg) is a toxic substance that causes oxidative damage to neurons. Vitamin C, a well-known antioxidant, can protect neurons from oxidative damage. In this study, we found that supplementation with L-ascorbic acid 2-phosphate (AA2P) could attenuate MeHg-induced apoptosis by reducing reactive oxygen species (ROS)-mediated DNA damage. AA2P also increased cell viability and decreased MeHg-induced apoptosis. Furthermore, it regulated gene expression in a contrary manner compared to MeHg. This study suggests that AA2P may be a potential treatment for MeHg neurotoxicity.
Review
Cell Biology
Artyom Y. Baev, Andrey Y. Vinokurov, Irina N. Novikova, Viktor V. Dremin, Elena V. Potapova, Andrey Y. Abramov
Summary: Neurodegenerative disorders are devastating diseases characterized by the loss of neurons in specific brain regions. Recent research has identified genes, toxins, and risk factors associated with these diseases, and has found similarities in the involvement of mitochondria, oxidative stress, and abnormal calcium signaling in neurons and astrocytes.
Article
Environmental Sciences
Wan-He Li, Zheng-Ting-Yan Xiang, An-Xin Lu, Su-Su Wang, Chong-Huai Yan
Summary: Manganese (Mn) is an essential trace element that maintains normal physiological functions, but overexposure to Mn can lead to multi-system disorders, especially neurotoxicity. This study investigated the modulation of the ROS-activated JNK/FOXO3a signaling pathway in Mn-induced apoptosis using a rat brain astrocyte cell line (CTX cells). The results showed that Mn decreased cell viability of CTX cells in a dose-dependent manner and induced apoptosis by altering the expression of apoptosis-related proteins. Treatment with Mn also resulted in elevated ROS levels and increased phosphorylation levels of JNK, while phosphorylation of FOXO3a was decreased. Depletion of ROS and inhibition of the JNK pathway prevented Mn-induced apoptosis. These findings provide insights into the neurotoxic mechanisms of Mn and potential therapeutic targets.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2023)
Article
Biochemistry & Molecular Biology
Xin Tan, Yong-feng Chen, Shi-ying Zou, Wei-jie Wang, Ning-ning Zhang, Zheng-Yu Sun, Wei Xian, Xiao-rong Li, Bi Tang, Hong-ju Wang, Qin Gao, Pin-fang Kang
Summary: The expression of ALDH2 is downregulated in diabetic myocardial I/R injury, and its activation improves cardiac hemodynamics and myocardial injury. ALDH2 regulates the dynamic balance of mitochondrial fusion and fission in hypoxia-reoxygenation model and maintains mitochondrial morphology stability. It also inhibits mitoPTP opening, reduces cell apoptosis and mitochondrial ROS levels, and activates the PI3K/AKT/mTOR pathway.
FREE RADICAL BIOLOGY AND MEDICINE
(2023)
Article
Biochemistry & Molecular Biology
Qian Gao, Zhong-Yuan Zhou, Ya-Ning He, Ming-Hui Dong, Zhao-Ning Wang, Hong-Mei Chen
Summary: This study evaluated the toxicity of BDE-47 towards RAW264.7 mouse macrophage cells and found that it caused a decrease in cell viability, an increase in apoptosis, and inhibition of phagocytosis. The mechanisms involved mitochondrial pathway-induced cell apoptosis and oxidative damage. Treatment with an antioxidant reversed the effects, while treatment with a ROS-inducer exacerbated them. These findings highlight the critical role of oxidative damage in BDE-47-induced suppression of immune function.
Review
Pharmacology & Pharmacy
Shaoyun Zhou, Qinwei Yu, Luyong Zhang, Zhenzhou Jiang
Summary: Mitochondria play multiple roles in cellular processes, acting as energy producers and biosynthetic centers. The opening of the mitochondrial permeability transition pore (mPTP) is a major contributor to mitochondrial dysfunction, leading to cellular damage or death. Cyclophilin D (CypD), a mitochondrial chaperone, has been identified as a key mediator of mPTP. Inhibiting CypD activity has shown to protect against diseases such as ischemia/reperfusion injury and neurodegenerative disorders.
CURRENT PHARMACEUTICAL DESIGN
(2023)
Review
Medicine, Research & Experimental
Rajalaxmi Behera, Veerta Sharma, Amarjot Kaur Grewal, Amit Kumar, Bhaskar Arora, Agnieszka Najda, Ghadeer M. Albadrani, Ahmed E. Altyar, Mohamed M. Abdel-Daim, Thakur Gurjeet Singh
Summary: Mitochondrial dysfunction is a fundamental cause of ischemia reperfusion (I/R) damage, which refers to the paradoxical progression of cellular dysfunction and death when blood flow is restored to previously ischemic tissues. The opening of mitochondrial permeability transition pores (MPTP) due to increased mitochondrial permeability is a key factor in I/R injury. The interaction between MPTP and mitoKATP and their roles in I/R injury are the focus of this review.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Biochemistry & Molecular Biology
James H. Schofield, Zachary T. Schafer
Summary: The relationship between mitophagy and ROS production is complex and not fully understood. This review discusses mtROS generation and their detrimental effects on cellular viability, along with the cellular defense mechanisms against oxidative stress. Furthermore, the prominent mechanisms governing mitophagy induction that bear on oxidative stress are explored.
ANTIOXIDANTS & REDOX SIGNALING
(2021)
Article
Biochemistry & Molecular Biology
Anberitha T. Matthews, Hitesh Soni, Katherine E. Robinson-Freeman, Theresa A. John, Randal K. Buddington, Adebowale Adebiyi
Summary: Doxorubicin (DOX), a chemotherapeutic agent, can induce fetal nephrotoxicity by inhibiting proliferation and inducing death of fetal pig glomerular mesangial cells (GMCs). DOX treatment reduces TRPC6 protein expression, leading to mitochondrial ROS generation and cell death in GMCs. The DOX-induced fetal pig GMC apoptosis is independent of TRPC6 upregulation but requires mtROS production.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Toxicology
Changcun Bai, Tingting Wei, Lingyue Zou, Na Liu, Xiaoquan Huang, Meng Tang
Summary: Recently, the increasing use of CdTe quantum dots in biomedicine has led to concerns regarding their biosafety. This study observed that exposure to CdTe quantum dots led to decreased cell viability and increased apoptosis rates in ND7/23 cells. The findings suggest that CdTe quantum dots induce apoptosis through the mitochondrial pathway. This research provides valuable insights for understanding the toxic mechanisms of CdTe quantum dots and reducing their adverse effects.
JOURNAL OF APPLIED TOXICOLOGY
(2022)
Review
Biochemistry & Molecular Biology
Chenbin Bian, Zhuangzhuang Zheng, Jing Su, Huanhuan Wang, Sitong Chang, Ying Xin, Xin Jiang
Summary: Radiotherapy failure and poor tumor prognosis are mainly caused by radioresistance. The relationship and mechanisms between mitochondrial metabolism and cancer radioresistance are not fully understood. However, mitochondria play a crucial role in regulating various biological reactions and influencing the radiation effects of malignancies. Therefore, targeting mitochondrial signaling pathways for the development of novel anticancer drugs holds promise.
Article
Engineering, Environmental
Guoliang Chen, Mingxing Wang, Panpan Zhu, Guixue Wang, Tingzhang Hu
Summary: Pyraoxystrobin (SYP-3343), a newly-invented strobilurin fungicide, exhibits high toxicity to aquatic organisms, particularly in zebrafish embryos, through affecting cell cycle, mitochondrial membrane potential, and reactive oxygen species generation. This toxicity is dose- and time-dependent, inducing apoptosis in zebrafish embryos.
JOURNAL OF HAZARDOUS MATERIALS
(2022)
Article
Chemistry, Multidisciplinary
Hulya Gizem Ozkan, Vanrajsinh Thakor, Hong-Gui Xu, Galyna Bila, Rostyslav Bilyy, Daria Bida, Martin Boettcher, Dimitrios Mougiakakos, Rainer Tietze, Andriy Mokhir
Summary: Elevated levels of reactive oxygen species (ROS) and deficient mitochondria are weak points of cancer cells. Designing highly potent anticancer drugs that target both ROS and mitochondria is a valid therapeutic strategy. However, limiting the drug effects to cancer cells without affecting normal ones remains a challenge. In this study, we developed novel aminoferrocene derivatives that are chemically stable in the presence of ROS, generate mitochondrial ROS in cancer cells but not normal cells, and exhibit anticancer effects in vivo.
CHEMISTRY-A EUROPEAN JOURNAL
(2022)
Review
Medicine, Research & Experimental
Wu Liu, Eskandar Qaed, Han Guo Zhu, Ma Xiao Dong, ZeYao Tang
Summary: PCr plays a significant role in maintaining cellular energy metabolism and preventing apoptosis by regulating mitochondrial respiration, enhancing ATP synthase and MitCK activities, and promoting these enzymatic reactions.
BIOMEDICINE & PHARMACOTHERAPY
(2021)