Cineole alleviates the BPA-inhibited NETs formation by regulating the p38 pathway-mediated programmed cell death

Chen, Lu; Tao, Dayong; Qi, Meng; Jiang, Zhihui; Xu, Shiwen

doi:10.1016/j.ecoenv.2022.113558

Cited by 14 publications

(5 citation statements)

References 41 publications

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“…NO is involved in nutritional deficiency and toxicity diseases. iNOS and NO levels in peripheral blood neutrophils of chickens were significantly elevated by BPA ( Chen et al, 2022 ). iNOS and HO-1d transcript and protein levels in rat liver were significantly elevated by BPF, but there was no effect on eNOS, which induced a nitrosative stress response (RNS) ( Linillos-Pradillo et al, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

“…Nitric oxide ( NO ) is an important messenger molecule catalytically produced by inducible nitric oxide synthase ( iNOS ), which can be involved in a variety of cellular signaling processes, and it also acts as a free radical participating in inflammatory responses and cytotoxicity ( Chen et al, 2022 ; Linillos-Pradillo et al, 2023 ). Interleukin-6 ( IL-6 ) signaling is important for immune cell recruitment and apoptosis, as well as inflammatory activation ( Campbell et al, 1993 ; Jones, 2005 ; Jones et al, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

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Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach

Wu,

Su,

et al. 2024

Poultry Science

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach

Wu,

Su,

et al. 2024

Poultry Science

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“…Many studies have shown that toxic exposure can cause oxidative stress and induce a series of toxic effects 48,49 . DEHP can aggravate mitochondrial damage and enhance cytotoxicity by increasing the production of ROS and promoting mitochondrial fragmentation 50 .…”

Section: Discussionmentioning

confidence: 99%

“…47 The purpose of this study is to investigate the effects Many studies have shown that toxic exposure can cause oxidative stress and induce a series of toxic effects. 48,49 DEHP can aggravate mitochondrial damage and enhance cytotoxicity by increasing the production of ROS and promoting mitochondrial fragmentation. 50 Low dose DEHP prenatal and lactation exposure can aggravate oxidative stress and behavioral defects in hippocampus of rats.…”

Section: Discussionmentioning

confidence: 99%

Di(2‐ethylhexyl) phthalate and microplastics cause necroptosis and apoptosis in hepatocytes of mice by inducing oxidative stress

Chen

Zhang

et al. 2023

Environmental Toxicology

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Di(2‐ethylhexyl) phthalate (DEHP) is a plasticizer and an endocrine disruptor. Microplastics (MPs) are pathogenic small plastic particles and abundant in the aqueous environment. The problem of residual hazards of plastic products is worthy of study, especially the joint exposure of a variety of plastic‐related products to the toxic effect. We used 200 mg/kg DEHP and 10 mg/L MPs to establish exposure model in vivo and 2 mM DEHP and 200 μg/L MPs to establish AML12 cell exposure model in vitro. In vivo study results showed that compared with the control group (NC) group, DEHP and MPs significantly increased the contents of malondialdehyde and hydrogen peroxide, and significantly decreased the contents of glutathione and the activity of superoxide dismutase, total antioxidant capacity, catalase and glutathione peroxidase. The level of oxidative stress was further aggravated after combined exposure. The reactive oxygen species level of AML12 exposed to DEHP and MPs in vitro was significantly higher than NC group, and the combined exposure was significantly higher than the single exposure. The in vivo and in vitro also confirmed that DEHP and MPs could significantly increase the mRNA and protein levels of apoptosis markers and necroptosis markers and there was an additive effect. After N‐acetylcysteine treatment in vitro, the above‐mentioned oxidative stress level and cell damage decreased significantly. This study provided a reference for advocating the reduction of the mixed use of plastic products, and provided a basis for preventing the harm of plastic products residues.

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“…BPA exposure has been shown to alter DNA methylation patterns and modify histone structure, resulting in changes in gene expression and potential health effects [12]. Other studies have also reported that exposure to BPA can induce cell death, disrupt mitochondrial function, and alter neurotransmitter signaling [25][26][27]. However, further research is necessary to fully elucidate the mechanisms behind these effects (Figure 3).…”

Section: Mechanisms Of Bisphenol a Toxicitymentioning

confidence: 99%

Bisphenol-A (BPA) Exposure as a Risk Factor for Non-Communicable Diseases

Maduabuchi Aja,

Victor Fasogbon,

Adomi Mbina

et al. 2024

Bisphenols - New Environmental, Pathophysiological and Social Perspectives [Working Title]

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Bisphenol-A (BPA) is a widely used chemical compound in the production of consumer items and building materials. Over the years, concerns have been raised about its potential adverse effects on human health. This chapter aims to explore the existing evidence regarding the association between BPA exposure and the risk of non-communicable diseases (NCDs). NCDs, such as cardiovascular diseases, diabetes, obesity, and certain types of cancer, are the leading causes of morbidity and mortality worldwide. Multiple studies have investigated the potential role of BPA in the development and progression of these diseases. Epidemiological studies have also provided evidence suggesting a link between BPA exposure and NCDs in humans. Several potential mechanisms have been proposed to explain the effects of BPA on NCDs, including its ability to mimic estrogenic activity and alter hormone signaling. A broader knowledge of the association between BPA and NCDs can inform public health policies and strategies aimed at reducing BPA exposure towards mitigating the burden of NCDs. In general, while the evidence regarding the association between BPA exposure and NCDs is still evolving, the existing literature suggests a potential link between BPA exposure and an increased risk of developing various non-communicable diseases.

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Cineole alleviates the BPA-inhibited NETs formation by regulating the p38 pathway-mediated programmed cell death

Cited by 14 publications

References 41 publications

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach

Di(2‐ethylhexyl) phthalate and microplastics cause necroptosis and apoptosis in hepatocytes of mice by inducing oxidative stress

Bisphenol-A (BPA) Exposure as a Risk Factor for Non-Communicable Diseases

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