Effects of phenanthrene on oxidative stress and inflammation in lung and liver of female rats

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Low molecular weight-Polycyclic aromatic hydrocarbons (LMW-PAHs) are ubiquitous environmental pollutants, which may contribute to respiratory diseases. However, studies of the relative mechanisms are limited. This study aimed to explore the effects of two LMW-PAHs [phenanthrene (Phe) and fluorene (Flu)], separately and as binary PAH mixture on oxidative stress and inflammation in A549 cells. Cell viability was firstly detected at various concentrations (200-800 μM) by Phe, Flu, and the mixture of Phe and Flu. ROS level, MDA content, SOD and CAT activities were then determined to evaluate oxidative damage. The protein and mRNA expressions of IL-6, TNF-α, TGF-β, and the protein content of SPA were further determined to evaluate inflammation. Results showed that Phe, Flu, and their mixture triggered ROS generation and induced abnormal productions of MDA, SOD, and CAT. And the protein and mRNA expressions of TNF-α and IL-6 were increased by Phe, Flu, and their mixture, respectively. In addition, SPA was also increased by Phe and Flu, while it was decreased by their mixture at 600 μM. The results demonstrated that Phe, Flu, and their mixture could induce oxidative stress and subsequent inflammation in A549 cells, while combined inflammatory response was stronger than single actions.

Section: Discussionsupporting

confidence: 79%

Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Oxidative stress and inflammatory effects in human lung epithelial A549 cells induced by phenanthrene, fluorene, and their binary mixture

Guo

Zhang

Wang

et al. 2020

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The effect of low molecular weight‐polycyclic aromatic hydrocarbons responsive hsa_circ_0039929/hsa‐miR‐15b‐3p_R‐1/FGF2 circuit on inflammatory response of A549 cells via the PI3K/AKT pathway and epithelial‐mesenchymal transition process

Huang

Wang

et al. 2022

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Inflammation is widely recognized as an essential inducer of epithelial‐mesenchymal transition (EMT). Meanwhile, competitive endogenous RNA (ceRNA) has been involved in a variety of disease processes. Therefore, the aim of the current study is to explore the regulation of ceRNA in the PI3K/AKT pathway and EMT mechanism in inflammatory response caused by low molecular weight‐polycyclic aromatic hydrocarbons (LMW‐PAHs). The A549 cells were treated with an equal mixture of phenanthrene (Phe) and fluorene (Flu), and total RNA was extracted for transcriptome sequencing. The target regulation of ceRNA hsa_circ_0039929/hsa‐miR‐15b‐3p_R‐1/FGF2 was further determined for mechanism study. The mixture of Phe and Flu significantly upregulated the expressions of hsa_circ_0039929 and FGF2, down‐regulated hsa‐miR‐15b‐3p_R‐1, activated the PI3K/AKT pathway and promoted EMT. Mechanically, the overexpression of hsa‐miR‐15b‐3p_R‐1 inhibited the expressions of hsa_circ_0039929 and FGF2, reversed the activation of PI3K/AKT signaling pathway by LMW‐PAHs, and blocked the occurrence of EMT progression. Furthermore, knockdown of hsa_circ_0039929 could promote the levels of hsa‐miR‐15b‐3p_R‐1, while inhibit the expression of FGF2. The effects of hsa_circ_0039929 knockdowns on PI3K/AKT pathways and EMT progress resembled the hsa‐miR‐15b‐3p_R‐1 overexpression. All above suggested that ceRNA hsa_circ_0039929/hsa‐miR‐15b‐3p_R‐1/FGF2 played an important role in the inflammation and EMT caused by LMW‐PAHs.

Molybdenum and cadmium co‐exposure promotesM1macrophage polarization through oxidative stress‐mediated inflammatory response and induces pulmonary fibrosis inShaoxing ducks (Anas platyrhyncha)

Huang

Luo

Guo

et al. 2022

High molybdenum (Mo) and cadmium (Cd) are harmful to the body, but pulmonary toxicity induced by Mo and Cd co‐exposure is unknown. To assess the combined impacts of Mo and Cd on fibrosis through M1 polarization in the lung of ducks, 80 healthy 8‐day‐old Shaoxing ducks (Anas platyrhyncha) were randomly assigned to 4 groups and fed with containing unequal doses of Mo or/and Cd diet. Lung tissues were collected on the 16th week. Results indicated that Mo or/and Cd significantly increased their contents in the lungs, and led to trace elements disorder and histological abnormality, and oxidative stress accompanied by promoting contents of H2O2 and MDA and decreasing activities of T‐SOD, GSH‐Px, and CAT, then activated the TLR4/NF‐κB/NLRP3 pathway accompanied by upregulating Caspase‐1, ASC, IL‐18, IL‐1β, TLR4, NF‐κB, and NLRP3 expression levels, and disrupted M1/M2 balance to divert toward M1, which evoked the TGF‐β/Smad2/3‐mediated fibrosis by elevating TGF‐β1, Smad2, Smad3, COL1A1, α‐SMA, and MMP2 expression levels, and decreasing Smad7 and TIMP2 expression levels. The changes of the combined group were most obvious. To sum up, the research demonstrated that Mo or/and Cd may cause macrophages to polarize toward M1 by oxidative stress‐mediated the TLR4/NF‐κB/NLRP3 pathway, then result in fibrosis through the TGF‐β1/Smad2/3 pathway in duck lungs. Mo and Cd may worsen lung damage.