Article
Biochemistry & Molecular Biology
Yixuan Zhang, Jianzhuang Wu, Yao Fu, Ranran Yu, Haochen Su, Qisi Zheng, Hao Wu, Siqi Zhou, Kun Wang, Jing Zhao, Shanshan Shen, Guifang Xu, Lei Wang, Chao Yan, Xiaoping Zou, Ying Lv, Shu Zhang
Summary: This study identified Hesperadin as a potent anti-cancer compound against pancreatic cancer (PC) by inhibiting cell growth and inducing apoptotic cell death. Mechanistic studies revealed that Hesperadin increased GADD45A expression via ATF4, leading to apoptosis. Immunohistochemical staining demonstrated the correlation between ATF4 and GADD45A expression. PC xenograft studies confirmed the inhibitory effect of Hesperadin on PC cell growth in vivo.
Article
Biochemistry & Molecular Biology
Yurong Fu, Yongcheng Jin, Yue Tian, Hao Yu, Ruqi Wang, Huiyu Qi, Bo Feng, Jing Zhang
Summary: The synergistic effect of ZEA and LPS aggravates cytotoxicity by increasing the accumulation of ROS and MDA, decreasing MMP and SOD levels, and reducing GSH levels. Additionally, ZEA and LPS promote cell apoptosis by activating ER stress and suppressing anti-apoptotic proteins.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Medicine, Research & Experimental
Yuxin Du, Laurie J. Demillard, Jun Ren
Summary: Cerebrovascular diseases such as stroke can lead to cardiac complications through mechanisms such as catecholamine surges, which increase the risk of heart damage.
Article
Biochemistry & Molecular Biology
Wangjuan Dai, Xiaofei Zou, Hongyan Jia, Yawen Peng, Boya La, Zhenjie Yan, Li Gao, Lianju Qin, Feiyang Diao, Xiang Ma, Yan Meng, Yugui Cui, Jiayin Liu
Summary: This study found that Prdx4 released by cumulus cells can repair meiotic defects in mouse oocytes and improve oocyte quality. Co-culturing immature oocytes with cumulus cells decreased oxidative stress and ER stress, leading to enhanced oocyte maturation.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Marine & Freshwater Biology
Wei Hu, Qing-Ling Zhu, Jia-Lang Zheng, Zheng-Yong Wen
Summary: Exposure to cadmium led to growth inhibition, increased cadmium accumulation, oxidative stress, and other negative effects in fish. However, fish exhibited compensatory adaptive responses to resist cadmium toxicity. Genes involved in metabolic pathways were dysregulated by cadmium, potentially contributing to the toxicity.
AQUATIC TOXICOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Lina Cao, Jingjing Zhang, Yan Du, Min Sun, Yue Xiang, Yulu Sheng, Xiangmei Ren, Jihong Shao
Summary: Sodium selenite (Na2SeO3) exhibits anti-tumor activity in MCF7 cells by inducing apoptosis and activating the endoplasmic reticulum stress pathway. Oxidative stress and endoplasmic reticulum stress interact to regulate the survival of cancer cells.
CHEMICO-BIOLOGICAL INTERACTIONS
(2021)
Article
Environmental Sciences
Qiaoni Hu, Jifang Zheng, Xiao Na Xu, Chaohao Gu, Wanting Li
Summary: Uranium contamination induces excessive intracellular reactive oxygen species (ROS) generation, which is considered as a possible mediator of kidney tubular cells injury and nephrotoxicity. This study found that U exposure triggers endoplasmic reticulum stress, apoptosis, and down-regulation of PI3K/AKT/mTOR signaling. Administration of antioxidant N-acetylcysteine (NAC) effectively blocks ROS generation, ER stress, and apoptosis, and reverses the down-regulation of phosphorylated PI3K induced by U exposure.
ENVIRONMENTAL TOXICOLOGY
(2022)
Article
Oncology
Jing Xu, Gang Bi, Qingya Luo, Yi Liu, Tao Liu, Lanfang Li, Qi Zeng, Qien Wang, Yufeng Wang, Jianhua Yu, Ping Yi
Summary: The study revealed that in human ovarian cancer, PHLDA1 modulates cell sensitivity to apoptosis through the endoplasmic reticulum stress response pathway, which is associated with disease stage, progression-free survival, and overall survival.
Article
Engineering, Environmental
Huanliang Liu, Wenqing Lai, Xiaohua Liu, Honglian Yang, Yanjun Fang, Lei Tian, Kang Li, Huipeng Nie, Wei Zhang, Yue Shi, Liping Bian, Susu Ding, Jun Yan, Bencheng Lin, Zhuge Xi
Summary: The research investigated the mechanism of hepatotoxicity and apoptosis caused by Nano-CuO through oxidative stress and ER-stress. Both in vivo and in vitro experiments confirmed that Nano-CuO induced oxidative stress, leading to ER-stress pathway activation and subsequently cell death.
JOURNAL OF HAZARDOUS MATERIALS
(2021)
Article
Biochemistry & Molecular Biology
Wenrong Feng, Shengyan Su, Changyou Song, Fan Yu, Jun Zhou, Jianlin Li, Rui Jia, Pao Xu, Yongkai Tang
Summary: High concentrations of copper pose a threat to aquatic animals, but the response mechanisms of crustaceans to Cu2+ exposure are not well understood. This study investigated the physiological and molecular changes in Chinese mitten crabs after Cu2+ exposure. The results showed that Cu2+ exposure decreased antioxidative capacity and promoted lipid peroxidation in different tissues. It also induced apoptosis and autophagy, and triggered an immune response. The toxicity of Cu2+ may be associated with the activation of ERK, AMPK, and TLR2-MyD88-NF-kappa B pathways.
Article
Chemistry, Medicinal
Yan Guo, Suxing Jin, Hao Yuan, Tao Yang, Kun Wang, Zijian Guo, Xiaoyong Wang
Summary: Mono-Pt kills cancer cells through a mitophagic pathway by stimulating endoplasmic reticulum stress and activating the unfolded protein response, severely impairing mitochondrial structure and function.
JOURNAL OF MEDICINAL CHEMISTRY
(2022)
Article
Biochemistry & Molecular Biology
Li Yang, Xing Wang, Yongfei Zhao, Ke Xue, Jiankang Liang, Xiaohan Wang, Jing Deng, Zhengjian Qi
Summary: In this study, an AIE-type strong endoplasmic reticulum-targeted luminogen (MTOQS) was developed. MTOQS efficiently produced reactive oxygen species (ROS) in cellular and non-cellular environments, effectively reducing levels of GSH and MDA in cancer cells. Through dual organelle oxidative stress, MTOQS altered cancer cell metabolism and culture environment, leading to apoptosis by damaging endoplasmic reticulum and mitochondria.
BIOORGANIC CHEMISTRY
(2023)
Review
Biochemistry & Molecular Biology
Shouji Matsushima, Junichi Sadoshima
Summary: Oxidative stress plays a critical role in the pathophysiology of myocardial ischemic-reperfusion (I/R) injury. NADPH oxidase (Nox) 2 and 4, major sources of reactive oxygen species (ROS) in cardiomyocytes, are upregulated in response to I/R. Suppression of Nox-derived ROS can prevent mitochondrial dysfunction and endoplasmic reticulum (ER) stress, leading to reduced myocardial I/R injury. However, minimal levels of ROS by either Nox2 or Nox4 are required for energy metabolism during I/R in order to preserve the levels of hypoxia-inducible factor-1 alpha (HIF-1 alpha) and peroxisome proliferator-activated receptor-alpha (PPAR alpha). Furthermore, extreme suppression of Nox activity may lead to reductive stress and paradoxical increases in ROS levels. Nox4 has different roles in organelles such as mitochondria, ER, and ER-mitochondria contact sites (MAMs). Mitochondrial Nox4 has a detrimental effect, causing ROS-induced mitochondrial dysfunction during I/R, whereas Nox4 in the ER and MAMs may potentially protect against I/R injury through regulation of autophagy and MAM function, respectively. Although Nox isoforms are potential therapeutic targets for I/R injury, it is important to optimize ROS levels and selectively inhibit Nox4 in mitochondria to maximize the effect of intervention.
Article
Environmental Sciences
Fu Cheng Yao, Yue Gu, Tian Jiang, Peng Fei Wang, Fei Biao Song, Zhi Zhou, Jun Long Sun, Jian Luo
Summary: Microplastics pollution is prevalent in coastal areas, posing a potential threat to marine organisms. In this study, the impact of polystyrene microplastics (PS-MPs) on Golden Pompano was investigated. The results showed that exposure to high concentrations of PS-MPs led to impaired growth, histopathological changes in the liver, oxidative stress, endoplasmic reticulum stress (ERS), apoptosis, metabolic alterations, and immune disturbance in the fish. These findings highlight the role of ERS in microplastics toxicology and reveal the adverse effects of microplastics on Golden Pompano.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2023)
Article
Environmental Sciences
Linjing Deng, Yongsheng Ma, Ping Ma, Yang Wu, Xu Yang, Qihong Deng
Summary: The study revealed that exposure to cooking oil fumes had significant toxic effects on the respiratory system of rats, including oxidative stress, activation of apoptosis factors, and endoplasmic reticulum stress. Vitamin E could effectively alleviate lung injury caused by exposure to cooking oil fumes.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2021)