The role of miR-222-2p in exosomes secreted by hexavalent chromium-induced premature senescent hepatocytes as a SASP component.

With the development of world industrialization, the environmental pollution of hexavalent chromium [Cr(VI)] is becoming an increasingly serious problem. In particular, the mechanisms by which long-term and low-dose exposure to Cr(VI) leading the development of related cancers are not well understood. As senescent cells gradually lose their ability to proliferate and divide, they will not be malignantly transformed.

Mechanism of NO-induced migraine in rats: The exploration of the role of miR-653-3p/IGF1 axis.

Migraine is a severely disabling primary neurological disorder. Although some studies have confirmed that nitrogen dioxide (NO) pollution increases the risk of migraine, and our previous study demonstrated the role of the channel protein transient receptor potential cation channel subfamily V member 1 (TRPV1) in NO-induced migraine, the underlying mechanisms have not been fully elucidated. This study aimed to explore the intrinsic toxicity mechanism of NO-induced migraines using transcriptome sequencing.

Ambient NO hinders neutrophil extracellular trap formation in rats: Assessment of the role of neutrophil autophagy.

NO has been known to impair immunity and exacerbate susceptibility to infectious diseases. However, scant notice has been taken of the effect of NO on neutrophils. Neutrophil extracellular traps (NETs) formation is necessary for NETosis development by neutrophils as an immune system against pathogens.

Spleen Toxicity of Organophosphorus Flame Retardant TDCPP in Mice and the Related Mechanisms.

Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) is an organophosphorus flame retardant that has been utilized in recent years as a primary replacement for polybrominated diphenyl ethers (PBDEs) in a wide variety of fire-sensitive applications. However, the impact of TDCPP on the immune system has not been fully determined. As the largest secondary immune organ in the body, the spleen is considered to be an important study endpoint for determining immune defects in the body.

Long-term exposure to ambient air pollutants and their interaction with physical activity on insomnia: A prospective cohort study.

Exposure to air pollution or lack of physical activity (PA) increases the risk of insomnia. However, evidence on joint exposure to air pollutants is limited, and the interaction of joint air pollutants and PA on insomnia is unknown. This prospective cohort study included 40,315 participants with related data from the UK Biobank, which recruited participants from 2006 to 2010.

Effect of propiconazole on neutrophil extracellular traps formation: Assessing the role of autophagy.

Propiconazole (Pcz) is a kind of triazole fungicide which has an important impact on the environment. With the extensive use of Pcz in agricultural production activities, the pesticides are left in soil, water, crops and food, and will enter the organisms in the form of residues. Neutrophils play a key role in the body's innate immunity against pathogens, and the formation of neutrophil extracellular traps (NETs) is an important way for neutrophils to exert their immune function.

Ambient NO exposure induces migraine in rats: Evidence, mechanisms and interventions.

Migraine is a complex neurological disorder with a high disability rate. Although the precipitating factors of migraine remain unclear, previous studies suggest that when there is excess nitrogen dioxide (NO) pollution in the atmosphere, the medical demand due to migraine attacks increases sharply. However, the main role of NO as a trigger for migraine is not yet well understood.

Hexavalent chromium triggers hepatocytes premature senescence via the GATA4/NF-κB signaling pathway mediated by the DNA damage response.

Hexavalent chromium [Cr(VI)] is a proven toxin, carcinogen and environmental pollutant. Oral intake of Cr(VI) has been shown to lead to an increasing incidence of primary hepatic carcinoma in the population. Cellular senescence is thought to be a natural barrier to malignant transformation of cells, but senescence-associated secretory phenotype (SASP) is secreted and regulated by senescent cells links cellular senescence to malignant transformation in a dynamic way.

Ambient NO exposure induced cardiotoxicity associated with gut microbiome dysregulation and glycerophospholipid metabolism disruption.

An average daily increase of 10 μg/m in NO concentrations could lead to an increased mortality in cardiovascular, cerebrovascular of 1.89%, 2.07%, but the mechanism by which NO contributes to cardiotoxicity is rarely reported.

Endogenous hydrogen sulfide counteracts polystyrene nanoplastics-induced mitochondrial apoptosis and excessive autophagy via regulating Nrf2 and PGC-1α signaling pathway in mouse spermatocyte-derived GC-2spd(ts) cells.

Nanoplastics (NaPs) has reported to accumulate in the testes and cause degeneration in the seminiferous tubules. Additionally, exogenous hydrogen sulfide (HS) is proposed to enhance tolerance to oxidative stress. The current work aimed to investigate the mechanisms of NaPs-induced reproductive toxicity in vitro and probable reproductive protection by endogenous HS.

Clusterin protects against Cr(VI)-induced oxidative stress-associated hepatotoxicity by mediating the Akt-Keap1-Nrf2 signaling pathway.

Hexavalent chromium [Cr(VI)] is a serious environmental pollutant that threatens human life. Cr(VI) is widely used in industrial processes such as metallurgy, leather processing, and electroplating, which can enter the human body through the respiratory or digestive tracts, thus causing a number of human disease, including inflammation and cancer. Although it has been confirmed that oxidative stress is one of the primary mechanism of liver injury caused by Cr(VI) exposure, the related toxic target and effective intervention measures have not been found.

Curcumin hinders PBDE-47-induced neutrophil extracellular traps release via Nrf2-associated ROS inhibition.

Polybrominated diphenyl ethers (PBDE-47), a kind of lipophilic persistent organic pollutants (POPs) brominated flame retardant, has been widely used in various consumer products. However, the toxicity of PBDE-47 on human immune system has not been well elucidated. Neutrophil extracellular traps (NETs) contribute to the innate immune responses, and the release of NETs is recognized as the most important part of the extracellular killing mechanism.

Hexavalent chromium inhibits the formation of neutrophil extracellular traps and promotes the apoptosis of neutrophils via AMPK signaling pathway.

As the most common heavy metal pollutant, hexavalent chromium [Cr(VI)] has caused serious environmental pollution and health damage. Although the toxic effect of Cr(VI) has been widely studied, and oxidative stress has been confirmed to be the main mechanism of its cytotoxicity, the toxicity of Cr(VI) to human immune system remains to be elucidated. Neutrophil extracellular traps (NETs) participate in the innate immune response, and the release of NETs is considered to be the most important part of the extracellular killing mechanism.

ERK/p38/ROS burst responses to environmentally relevant concentrations of diphenyl phosphate-evoked neutrophil extracellular traps formation: Assessing the role of autophagy.

Organophosphorus compounds were proposed to impair immune surveillance and increase the total burden of pathogens. However, scarce attention has been paid to the effects of organophosphate flame retardants (OPFRs) on neutrophils. Previous literature outlined that neutrophil extracellular traps (NETs) death (NETosis) is associated with autophagy-related signaling.

Polystyrene microplastics trigger hepatocyte apoptosis and abnormal glycolytic flux via ROS-driven calcium overload.

Human health could be affected by the spread of microplastics in the food chain. Our previous research has indicated that microplastics accumulated in the liver and subsequently induce oxidative damage. However, the molecular events linking oxidative stress to calcium ion (Ca) signaling during microplastics stress remains elusive.

Clusterin inhibits Cr(VI)-induced apoptosis via enhancing mitochondrial biogenesis through AKT-associated STAT3 activation in L02 hepatocytes.

Improper treatment of a large amount of industrial waste makes hexavalent chromium [Cr(VI)] seriously pollute the atmosphere, soil and water, and enter the food chain, seriously affecting the health of workers and local residents. We previously proved that Clusterin (CLU) can inhibit the apoptosis of L02 hepatocytes induced by Cr(VI) through mitochondrial pathway, but the associated molecular mechanism has not been further studied. Mitochondrial biogenesis is an important step in mitochondrial damage repair, but the mechanism of mitochondrial biogenesis in Cr(VI)-induced liver toxicity is still unclear.

Role of Clusterin/NF-κB in the secretion of senescence-associated secretory phenotype in Cr(VI)-induced premature senescent L-02 hepatocytes.

Hexavalent chromium [Cr(VI)] and its compounds have caused serious environmental pollution and health damage. Senescent cells can actively change the surrounding environment by secreting some factors, which are called senescence associated secretory phenotype (SASP). Our previous work has confirmed that premature senescent hepatocytes induced by Cr(VI) expressed high level of Clusterin (CLU) and secrete interleukin-6 (IL-6) and IL-8.

The role of PKA/PP2B-mediated Drp1 phosphorylation and the subsequent EGFR inhibition in Cr(VI)-induced premature senescence.

In recent years, frequent hexavalent chromium [Cr(VI)] pollution incidents have severely damaged the ecology and endangered the public health. It is well known that cell senescence could promote the carcinogenesis, thus the related research on the occurrence of premature senescence is of great significance to the elucidation of the carcinogenic mechanism of Cr(VI). We previously confirmed that long-term low-dose Cr(VI) exposure induced premature senescence, but the key molecular events that determine the occurrence of premature senescence are still unclear.

Clusterin alleviates Cr(VI)-induced mitochondrial apoptosis in L02 hepatocytes via inhibition of Ca-ROS-Drp1-mitochondrial fission axis.

Hexavalent chromium [Cr(VI)] is ubiquitous in the environment and is commonly used in various industrial processes. Clusterin (CLU) is an extracellular chaperone protein which exerts the anti-apoptotic function. In this study, we aimed to explore the effect of CLU on Cr(VI)-induced mitochondrial fission and apoptosis.