Cadmium perturbed lipid profile and induced liver dysfunction in mice through phosphatidylcholine remodeling and promoting arachidonic acid synthesis and metabolism

Gu, Jie; Kong, Anqi; Guo, Chuanzhi; Liu, Junlin; Li, Kongdong; Ren, Zhen; Zhou, Yang; Tang, Min; Shi, Haifeng

doi:10.1016/j.ecoenv.2022.114254

Cited by 28 publications

(6 citation statements)

References 44 publications

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“…These cellular effects of Cd exposure are associated with the induction of lipid metabolism alterations and oxidative stress, which have been documented in in vitro studies on human and animal liver cells [13][14][15][16][17][18][19][20][21] as well as in vivo in animal models of chronic exposure to Cd [21,23]. Alterations of the cellular lipidome recently characterized in mouse liver and human hepatocarcinoma cells demonstrate that Cd toxicity induces specific changes in membrane phospholipids, especially in phosphatidylcholine synthesis and remodeling, also increasing the relative abundance of arachidonic acid residues in complex lipids [43], which is a characteristic lipidomic hallmark of inflammation and a potential therapeutic target of human fatty liver disease [44].…”

Section: Discussionmentioning

confidence: 96%

Melatonin as a Repairing Agent in Cadmium- and Free Fatty Acid-Induced Lipotoxicity

Migni,

Mancuso,

Baroni

et al. 2023

Biomolecules

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(1) Background: Cadmium (Cd) is a potentially toxic element with a long half-life in the human body (20–40 years). Cytotoxicity mechanisms of Cd include increased levels of oxidative stress and apoptotic signaling, and recent studies have suggested that these aspects of Cd toxicity contribute a role in the pathobiology of non-alcoholic fatty liver disease (NAFLD), a highly prevalent ailment associated with hepatic lipotoxicity and an increased generation of reactive oxygen species (ROS). In this study, Cd toxicity and its interplay with fatty acid (FA)-induced lipotoxicity have been studied in intestinal epithelium and liver cells; the cytoprotective function of melatonin (MLT) has been also evaluated. (2) Methods: human liver cells (HepaRG), primary murine hepatocytes and Caco-2 intestinal epithelial cells were exposed to CdCl2 before and after induction of lipotoxicity with oleic acid (OA) and/or palmitic acid (PA), and in some experiments, FA was combined with MLT (50 nM) treatment. (3) Results: CdCl2 toxicity was associated with ROS induction and reduced cell viability in both the hepatic and intestinal cells. Cd and FA synergized to induce lipid droplet formation and ROS production; the latter was higher for PA compared to OA in liver cells, resulting in a higher reduction in cell viability, especially in HepaRG and primary hepatocytes, whereas CACO-2 cells showed higher resistance to Cd/PA-induced lipotoxicity compared to liver cells. MLT showed significant protection against Cd toxicity either considered alone or combined with FFA-induced lipotoxicity in primary liver cells. (4) Conclusions: Cd and PA combine their pro-oxidant activity to induce lipotoxicity in cellular populations of the gut–liver axis. MLT can be used to lessen the synergistic effect of Cd-PA on cellular ROS formation.

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Section: Discussionmentioning

confidence: 96%

Melatonin as a Repairing Agent in Cadmium- and Free Fatty Acid-Induced Lipotoxicity

Migni,

Mancuso,

Baroni

et al. 2023

Biomolecules

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“… Miyashita (2014) showed that higher levels of DHA eggs are more tend to oxidize compared with normal eggs, which was consistent with our findings. Excessive ARA can lead to oxidative stress and affect the levels of PGE2 and TxB3 via the cyclooxygenase pathway ( Gu et al, 2022 ). Luo et al (2023) reported that the levels of the PGE2 and TxB3 were decreased in the oxidation process of egg yolk during spray drying and subsequently accelerated storage, the change of PGE2 was the same as our results.…”

Section: Discussionmentioning

confidence: 99%

Quantitative lipidomics reveals the changes of lipids and antioxidant capacity in egg yolk from laying hens with fatty liver hemorrhagic syndrome

Guo,

Zhang,

You

et al. 2024

Poultry Science

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“…An increase in fluvastatin levels can inhibit steatosis and steatohepatitis [ 49 ]. Besides the above metabolic pathways, significantly different metabolites between HFD and LBO were related to other metabolic pathways, such as tyrosine metabolism [ 50 ], arachidonic acid metabolism [ 51 ], and thiamine metabolism [ 52 ], which were associated with liver injury. These altered metabolic pathways predicted that the LBO treatment could exert a therapeutic effect by improving intestinal flora and metabolite disturbances in HFD-induced mice.…”

Section: Discussionmentioning

confidence: 99%

Lycium barbarum Oligosaccharides Alleviate Hepatic Steatosis by Modulating Gut Microbiota in C57BL/6J Mice Fed a High-Fat Diet

Zhang

et al. 2023

Foods

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High-fat diets (HFD) can promote the development of hepatic steatosis by altering the structure and composition of gut flora. In this study, the potential therapeutic mechanism of Lycium barbarum oligosaccharide (LBO) against hepatic steatosis was investigated by analyzing the changes in the intestinal flora and metabolites in mice. Mice on an HFD were administered LBO by gavage once daily for a continuous period of eight weeks. Compared with the HFD group, the levels of triglyceride (TG), alanine aminotransferase (ALT) in the serum, and hepatic TG were significantly reduced in the LBO group, and liver lipid accumulation was obviously improved. In addition, LBO could regulate the HFD-induced alteration of intestinal flora. The HFD increased the proportion of Barnesiellaceae, Barnesiella, and CHKCI001. LBO increased the proportion of Dubosiella, Eubacterium, and Lactobacillus. LBO also altered the fecal metabolic profile. Significantly different metabolites between LBO and the HFD, such as taurochenodeoxycholate, taurocholate, fluvastatin, and kynurenic acid, were related to the cholesterol metabolism, bile acid metabolism, and tryptophan metabolic pathways. In light of the above, LBO can alleviate HFD-induced NAFLD by modulating the components of the intestinal flora and fecal metabolites.

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Cadmium perturbed lipid profile and induced liver dysfunction in mice through phosphatidylcholine remodeling and promoting arachidonic acid synthesis and metabolism

Cited by 28 publications

References 44 publications

Melatonin as a Repairing Agent in Cadmium- and Free Fatty Acid-Induced Lipotoxicity

Melatonin as a Repairing Agent in Cadmium- and Free Fatty Acid-Induced Lipotoxicity

Quantitative lipidomics reveals the changes of lipids and antioxidant capacity in egg yolk from laying hens with fatty liver hemorrhagic syndrome

Lycium barbarum Oligosaccharides Alleviate Hepatic Steatosis by Modulating Gut Microbiota in C57BL/6J Mice Fed a High-Fat Diet

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