ROS and diseases: role in metabolism and energy supply

Yang, Shenshu; Lian, Gaojian

doi:10.1007/s11010-019-03667-9

Cited by 444 publications

(304 citation statements)

References 99 publications

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“…Usually, the intracellular ROS levels in cells are high when the lipid content is also high ( 131 ). ROS are important signaling molecules that act as a ligands or activate multiple cellular signaling pathways, such as heat shock factor protein 1, NF-κB, p53, PI3K-AKT and ERK/JNK/p38, thereby affecting cellular carbohydrate metabolism, mitochondrial function, apoptosis and necrosis, proliferation and cancer cell infiltration ( 132 – 135 ). At present, studies have found that ROS affect the formation and degradation of cellular lipids ( 12 , 23 , 64 , 136 ).…”

Section: Effects Of Lipid Droplets On Cellular Stress and Apoptosismentioning

confidence: 99%

Implications of lipid droplets in lung cancer: Associations with drug resistance (Review)

Jin

Yuan

2020

Oncol Lett

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Cancer cells usually show different metabolic patterns compared with healthy cells due to the reprogramming of metabolic processes. The process of lipid metabolism undergoes notable changes, leading to the accumulation of lipid droplets in cells. Additionally, this phenotype is considered an important marker of cancer cells. Lipid droplets are a highly dynamic type of organelle in the cell, which is composed of a neutral lipid core, a monolayer phospholipid membrane and lipid droplet-related proteins. Lipid droplets are involved in several biological processes, including cell proliferation, apoptosis, lipid metabolism, stress, immunity, signal transduction and protein trafficking. Epidermal growth factor receptor (EGFR)-activating mutations are currently the most effective therapeutic targets for non-small cell lung cancer. Several EGFR tyrosine kinase inhibitors (EGFR-TKIs) that target these mutations, including gefitinib, erlotinib, afatinib and osimertinib, have been widely used clinically. However, the development of acquired resistance has a major impact on the efficacy of these drugs. A number of previous studies have reported that the expression of lipid droplets in the tumor tissues of patients with lung cancer are elevated, whereas the association between elevated numbers of lipid droplets and drug resistance has received little attention. The present review describes the potential association between lipid droplets and drug resistance. Furthermore, the mechanisms and implications of lipid droplet accumulation in cancer cells are analyzed, as wells as the mechanism by which lipid droplets suppress endoplasmic reticulum stress and apoptosis, which are essential for the development and treatment of lung cancer. Contents

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Section: Effects Of Lipid Droplets On Cellular Stress and Apoptosismentioning

confidence: 99%

Implications of lipid droplets in lung cancer: Associations with drug resistance (Review)

Jin

Yuan

2020

Oncol Lett

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“…One of the factors that plays a complex role in these diseases is reactive oxygen species (ROS). Normally ROS are generated in the mitochondrial respiratory chain [ 3 ]. Excessive ROS induce oxidative stress causing lipid peroxidation that can lead to brain dysfunction and death [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Extracts from Tiger Milk Mushroom Lignosus rhinocerus Against Glutamate-Induced Toxicity in HT22 Hippocampal Neuronal Cells and Neurodegenerative Diseases in Caenorhabditis elegans

Kittimongkolsuk

Pattarachotanant

Chuchawankul

et al. 2021

Biology

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Despite the Tiger Milk Mushroom Lignosus rhinocerus (LR) having been used as a traditional medicine, little is known about the neuroprotective effects of LR extracts. This study aims to investigate the neuroprotective effect of three extracts of LR against glutamate-induced oxidative stress in mouse hippocampal (HT22) cells as well as to determine their effect in Caenorhabditis elegans. In vitro, we assessed the toxicity of three LR extracts (ethanol extract (LRE), cold-water extract (LRC) and hot-water extract (LRH)) and their protective activity by MTT assay, Annexin V-FITC/propidium iodide staining, Mitochondrial Membrane Potential (MMP) and intracellular ROS accumulation. Furthermore, we determined the expression of antioxidant genes (catalase (CAT), superoxide dismutase (SOD1 and SOD2) and glutathione peroxidase (GPx)) by qRT-PCR. In vivo, we investigated the neuroprotective effect of LRE, not only against an Aβ-induced deficit in chemotaxis behavior (Alzheimer model) but also against PolyQ40 formation (model for Morbus Huntington) in transgenic C. elegans. Only LRE significantly reduced both apoptosis and intracellular ROS levels and significantly increased the expression of antioxidant genes after glutamate-induced oxidative stress in HT22 cells. In addition, LRE significantly improved the Chemotaxis Index (CI) in C. elegans and significantly decreased PolyQ40 aggregation. Altogether, the LRE exhibited neuroprotective properties both in vitro and in vivo.

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“…CCL4 is metabolized by liver CYPs to CCL 3• free radicals and lead to lipid peroxidation and oxidative stress. In normal condition, ROS is generated and eliminated by antioxidant defense system 23 . Cells can response to oxidative stress when exposed to ROS and electrophilic chemicals by expression of protective proteins to avoid harm to cells.…”

Section: Discussionmentioning

confidence: 99%

Tert-butylhydroquinone mitigates Carbon Tetrachloride induced Hepatic Injury in mice

Zhang

et al. 2020

Int. J. Med. Sci.

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Tert-butylhydroquinone (tBHQ) is an antioxidant compound that exhibits cytoprotective effect in many tissues under pathological condition. However, its role in carbon tetrachloride (CCL4) induced liver injury is still unclear. Here we established a carbon tetrachloride induced hepatic injury model in mice to determine whether tBHQ can mitigate CCL4 induced liver damage. In our study, we found tBHQ exhibited protective effects in CCL4 treated mice model. TBHQ markedly improved hepatic function and decreased hepatic histopathological damage in vivo. In addition, tBHQ reduced levels of pro-inflammatory cytokines in mice model. Moreover, tBHQ mitigated apoptosis of hepatocytes, oxidative stress and lipid peroxidation in vivo and in vitro. We also found the possible mechanism of protective effects of tBHQ was associated with activation of Nrf2/ heme oxygenase-1 (HO-1) pathway. In conclusion, our study revealed tBHQ can be a potential therapeutic drug in treatment of acute hepatic injury.

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ROS and diseases: role in metabolism and energy supply

Cited by 444 publications

References 99 publications

Implications of lipid droplets in lung cancer: Associations with drug resistance (Review)

Implications of lipid droplets in lung cancer: Associations with drug resistance (Review)

Neuroprotective Effects of Extracts from Tiger Milk Mushroom Lignosus rhinocerus Against Glutamate-Induced Toxicity in HT22 Hippocampal Neuronal Cells and Neurodegenerative Diseases in Caenorhabditis elegans

Tert-butylhydroquinone mitigates Carbon Tetrachloride induced Hepatic Injury in mice

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