Subchronic exposure to CeCl promotes macrophage ferroptosis and atherosclerotic plaque formation by inhibiting the Keap1/Nrf2/GPX4 pathway.

Cerium chloride (CeCl), a prevalent by-product of rare earth mining, accumulates in the biota and environment of mining regions, including plants, animals, water resources, and air, posing potential health risks to local residents. Atherosclerosis (AS) is the pathological basis of cardiovascular disease. However, the relationship between subchronic CeCl exposure and AS progression, along with the underlying regulatory mechanisms by which CeCl modulates AS, remains unclear.

Impact of multi-metal exposure on blood pressure: a mediation analysis through oxidative stress markers in China's Southern Jiangxi Province.

Hypertension is a prevalent condition that contributes significantly to the global disease burden. Recent research endeavors have been investigating the potential causal link between metal exposure and the development of hypertension, yet consensus remains elusive. Nevertheless, studies examining the interplay among metal exposure, hypertension, and oxidative stress are relatively limited.

Pollution and health risk assessment of rare earth elements in soil, water and vegetables from an ion-adsorption rare earth mining area in Ganzhou, China.

Rare earth elements (REEs) are increasingly recognized as significant environmental pollutants due to their environmental persistence, bioaccumulation, and chronic toxicity. This study assessed REEs pollution in soil, water, and vegetables in an ion-adsorption rare earth mining area in Ganzhou, and evaluated the associated health risks to the local population. Results indicated that the REEs content in soil ranged from 168.

Dose-dependent effects of hydroquinone on liver injury and lipid dysregulation based on SCD1/AMPK signaling pathway in C57BL/6 mice.

Hydroquinone (HQ) is extensively utilized in various industrial applications and as a dermatological agent; however, its metabolic processes and toxicological effects, particularly in the liver, remain insufficiently understood. This study aimed to investigate the impact of different doses of HQ on liver injury and lipid metabolism in C57BL/6 mice, with a specific focus on the SCD1/AMPK signaling pathway. We administered HQ at doses of 0, 12.

Yttrium chloride induces ferroptosis in cardiomyocytes via iron accumulation and triggers cardiac lipid peroxidation and inflammation that cause heart adverse events in mice.

The growing presence of yttrium (Y) in the environment raises concern regarding its safety and toxicity. However, limited toxicological data are available to determine cardiotoxicity of Y and its underlying mechanisms. In the present study, yttrium chloride (YCl) intervention with different doses was performed in male Kunming mice for the toxicological evaluation of Y in the heart.

A Time Series Study for Effects of PM on Coronary Heart Disease in Ganzhou, China.

Objective: To investigate the effect of PM10 exposure in low concentration areas on the daily hospitalized patients with coronary heart disease. Methods: Daily air quality monitoring data, meteorological monitoring data and daily hospitalization data of coronary heart disease during 2019−2021 in Ganzhou, China were collected. Generalized additive model and distributed lag nonlinear model were used to evaluate the association between environmental PM10 and daily hospital visits for coronary heart disease.

Yttrium chloride-induced cytotoxicity and DNA damage response via ROS generation and inhibition of Nrf2/PPARγ pathways in H9c2 cardiomyocytes.

Increasing exploration of rare-earth elements (REEs) has resulted in a high REEs' exposure risk. Owing to their persistence and accumulation of REEs in the environment, their adverse effects have caused widespread concern. However, limited toxicological data are available for the adverse effects of yttrium (Y) and its underlying mechanisms of action.

Extreme temperatures and cardiovascular mortality: assessing effect modification by subgroups in Ganzhou, China.

Background: Many people die from cardiovascular diseases each year, and extreme temperatures are regarded as a risk factor for cardiovascular deaths. However, the relationship between temperature and cardiovascular deaths varies in different regions because of population density, demographic inequality, and economic situation, and the evidence in Ganzhou, China is limited and inconclusive.

Objective: This study aimed to assess extreme temperature-related cardiovascular mortality and identify the potential vulnerable people.

Sodium arsenite induces spatial learning and memory impairment associated with oxidative stress and activates the Nrf2/PPARγ pathway against oxidative injury in mice hippocampus.

Arsenic (As) is a ubiquitous environmental and industrial toxin with known correlates of oxidative stress and cognitive deficits in the brain. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcriptional factor that represents a central cellular antioxidant defense mechanism and transcribes many antioxidant genes. Peroxisome proliferator-activated receptor-gamma (PPARγ) is a well-known nuclear receptor to regulate lipid metabolism in many tissues, and it has been also associated with the control of oxidative stress, neuronal death, neurogenesis and differentiation.

Loss of FoxO3a prevents aortic aneurysm formation through maintenance of VSMC homeostasis.

Vascular smooth muscle cell (VSMC) phenotypic switching plays a critical role in the formation of abdominal aortic aneurysms (AAAs). FoxO3a is a key suppressor of VSMC homeostasis. We found that in human and animal AAA tissues, FoxO3a was upregulated, SM22α and α-smooth muscle actin (α-SMA) proteins were downregulated and synthetic phenotypic markers were upregulated, indicating that VSMC phenotypic switching occurred in these diseased tissues.

Regulation of Wnt Singaling Pathway by Poly (ADP-Ribose) Glycohydrolase (PARG) Silencing Suppresses Lung Cancer in Mice Induced by Benzo(a)pyrene Inhalation Exposure.

Benzo(a)pyrene (BaP) is a polycyclic aromatic hydrocarbon that specifically causes cancer and is widely distributed in the environment. Poly (ADP-ribosylation), as a key post-translational modification in BaP-induced carcinogenesis, is mainly catalyzed by poly (ADP-ribose) glycohydrolase (PARG) in eukaryotic organisms. Previously, it is found that PARG silencing can counteract BaP-induced carcinogenesis , but the mechanism remained unclear.

Protective Effects of Aqueous Extracts of against Hydroquinone-Induced Toxicity in Hepatic L02 Cells.

Hydroquinone (HQ) is widely used in food stuffs and is an occupational and environmental pollutant. Although the hepatotoxicity of HQ has been demonstrated both in vitro and in vivo, the prevention of HQ-induced hepatotoxicity has yet to be elucidated. In this study, we focused on the intervention effect of aqueous extracts of (FLJ) on HQ-induced cytotoxicity.

Sema 3A as a biomarker of the activated mTOR pathway during hexavalent chromium-induced acute kidney injury.

Semaphorin 3A (sema 3A) is one of a class of secretory proteins belonging to a family of axon-directed factors found in podocytes, distal tubules, and collecting tubes of the kidney. It is considered to be a potential target molecule involved in the mammalian target of the rapamycin (mTOR) pathway in renal injury or renal diseases, but it has an unknown role in the course of hexavalent chromium-Cr(VI) induced nephrotoxicity. In the present study, an acute kidney injury (AKI) model in rats or cultured tubular epithelial HK-2 cells was employed for Cr(VI) exposure alone or in combination with rapamycin (Rap) or N-acetyl-l-cysteine (NAC) or recombinant sema 3A.

Differently expressed long noncoding RNAs and mRNAs in TK6 cells exposed to low dose hydroquinone.

Previous studies have shown that long noncoding RNAs (lncRNAs) were related to human carcinogenesis and might be designated as diagnosis and prognosis biomarkers. Hydroquinone (HQ), as one of the metabolites of benzene, was closely relevant to occupational benzene poisoning and occupational leukemia. Using high-throughput sequencing technology, we investigated differences in lncRNA and mRNA expression profiles between experimental group (HQ 20 μmol/L) and control group (PBS).

Poly(ADP-ribose) glycohydrolase silencing down-regulates TCTP and Cofilin-1 associated with metastasis in benzo(a)pyrene carcinogenesis.

Benzo(a)pyrene (BaP) is a ubiquitously distributed environmental pollutant. BaP is a known carcinogen and can induce malignant transformation of rodent and human cells. Many evidences suggest that inhibitor of poly(ADP-ribose) glycohydrolase (PARG) is potent anticancer drug candidate.

[Investigation of the action mechanisms of poly-ADP-ribosylation in hexavalent chromium induced cell damage].

Objective: To investigate the effect of poly-ADP-ribosylation in hexavalent chromium Cr(VI) induced cell damage.

Methods: The study object, poly (ADP-ribose) glycohydrolase (PARG) deficient human bronchial epithelial cells (16HBE cells), was constructed previously by our research group. Normal 16HBE cells and PARG-deficient cells were treated with different doses of Cr (VI) for 24 h to compare the differences to Cr (VI) toxicity, meanwhile set up the solvent control group.

Role of poly(ADP-ribose) glycohydrolase silencing in DNA hypomethylation induced by benzo(a)pyrene.

Benzo(a)pyrene (BaP) is a known carcinogen cytotoxic which can trigger extensive cellular responses. Many evidences suggest that inhibitors of poly(ADP-ribose) glycohydrolase (PARG) are potent anticancer drug candidates. However, the role of PARG in BaP carcinogenesis is less understood.

[Effect of poly-ADP-ribosylation on the alteration of DNA methylation level of human bronchial epithelial cells induced by Cr (VI)].

Objective: To reveal the role of poly-ADP-ribosylation and DNA methylation in carcinogenic process induced induced by Cr (VI), and to discuss the relations between them.

Methods: The pre-established Poly (ADP-ribose) glycohydrolase (PARG) deficient cells and 16HBE cells were treated with different concentrations of Cr (VI), and the changes of total genomic DNA methylation level in different groups were detected by methylation immunofluorescent detection, as well as the changes of the activity of methyltransferases. Moreover, RT-PCR and western blotting method were applied to analyze the changes of expression of DNMT1, DNMT3a, DNMT3b and MBD2, upon the protein level.

Effect of low dose bisphenol A on the early differentiation of human embryonic stem cells into mammary epithelial cells.

It has been previously reported that bisphenol A (BPA) can disturb the development of mammary structure and increase the risk of breast cancer in experimental animals. In this study, an in vitro model of human embryonic stem cell (hESC) differentiation into mammary epithelial cells was applied to investigate the effect of low dose BPA on the early stages of mammogenesis. A newly established hESC line was directionally differentiated into mammary epithelial cells by a well-established three-dimensional (3D) culture system.

Down-regulation of Polη expression leads to increased DNA damage, apoptosis and enhanced S phase arrest in L-02 cells exposed to hydroquinone.

DNA polymerase eta (Polη), the product of the xeroderma pigmentosum variant gene, is required for translesion DNA synthesis, and plays a pivotal role in preventing genome instability after DNA damage induced by genotoxic agents. Studies have previously suggested a link between Polη and susceptibility to hydroquinone (HQ)-induced toxicity. To further address the role of Polη in the response of L-02 cells to HQ, we employed RNA interference to silence Polη expression in L-02 cells and examined the susceptibility of these Polη-deficient cells to the toxic effects of HQ.

Cr(VI) induces the decrease of ATP level and the increase of apoptosis rate mediated by ROS or VDAC1 in L-02 hepatocytes.

The present study explored the ability of the voltage-dependent anion channel 1 (VDAC1) mRNA and ROS levels to modulate the effects of hexavalent chromium Cr(VI) on the adenosine triphosphate (ATP) level and the rate of apoptotic cell death. Cultured L-02 cells were pretreated with 20mM N-acetyl-cysteine (NAC) for 24h or transiently transfected with small interfering RNAs targeting VDAC1 (siVDAC1) for 48h; cells that were not pretreated were used as the control. The cells were subsequently treated with 0, 2, 8, or 32μM Cr(VI) for 24h.

Chi-square analysis of the reduction of ATP levels in L-02 hepatocytes by hexavalent chromium.

This study explored the reduction of adenosine triphosphate (ATP) levels in L-02 hepatocytes by hexavalent chromium (Cr(VI)) using chi-square analysis. Cells were treated with 2, 4, 8, 16, or 32 μM Cr(VI) for 12, 24, or 36 h. Methyl thiazolyl tetrazolium (MTT) experiments and measurements of intracellular ATP levels were performed by spectrophotometry or bioluminescence assays following Cr(VI) treatment.

Role of poly(ADP-ribose) glycohydrolase in the regulation of cell fate in response to benzo(a)pyrene.

Poly(ADP-ribosyl)ation is a crucial regulator of cell fate in response to genotoxic stress. Poly(ADP-ribosyl)ation plays important roles in multiple cellular processes, including DNA repair, chromosomal stability, chromatin function, apoptosis, and transcriptional regulation. Poly(ADP-ribose) (PAR) degradation is carried out mainly by poly(ADP-ribose) glycohydrolase (PARG) enzymes.