NEUROTOXICOLOGY
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2015
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IF 3.379
Lihua Hu,Chuanyang Su,Xiufang Song,Qiong Shi,Juanli Fu,Xiaomin Xia,Demei Xu,Erqun Song,Yang Song
Although there are few studies suggested PCP exposure induced developmental and behavioral disorders, however, the occurrence of neurotoxicity and PCP has not been firmly established. Tetrachlorobenzoquinone (TCBQ) is a reactive metabolite of environmental pollutant pentachlorophenol (PCP). To the best of our knowledge, there has no information regarding to the neurological toxic effect of TCBQ available. Here, we demonstrated that TCBQ induces cytotoxicity in pheochromocytoma PC12 cell line, and the mode-of-action analysis indicated the involvement of apoptotic signalings, such as the activation of caspase family proteins, the increased expressions of Fas and Fas-associated death domain (FADD), the loss of mitochondrial membrane potential (MMP), the release of cytochrome c (Cyt c ) and the cleavage of the caspase substrates poly(ADP-ribose) polymerase (PARP). BI-6C9, a specific BH3-interacting domain death agonist (Bid) inhibitor, repressed TCBQ-induced Bid truncation, along with the activation of caspase 3 and the release of Cyt c , suggested the cross-talk of extrinsic and intrinsic apoptotic signalings. Furthermore, the inhibition of caspase 8 impaired TCBQ-induced the activation of caspase 3, as well as the release of Cyt c and the cleavage of Bid, suggesting caspase 8 acting as the upstream molecule of Bid, and TCBQ-induced apoptosis is initiated via caspase 8, leads to the activation of caspase 9/3 through Bid-mediated amplification loop. Finally, the pretreatment of antioxidant NAC ameliorated Fas, FADD and caspase 8/3 expressions, which illustrated that TCBQ-induced apoptotic signaling is ROS dependent. Taken together, these results indicated that the cleavage of Bid may play an important role in TCBQ-induced neurotoxicity which promotes the cross-talk of extrinsic and intrinsic apoptotic signalings in PC12 cells.
研究领域:
毒理学
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神经科学
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细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INDUSTRIAL CROPS AND PRODUCTS
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2024
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IF 5.6
Peixiao Sun,Hongjian Zhang,Xiaoli Li,Yang Leng,Bin Li,Zhao Wang,Miaojun Xu
With the rapid progress of electronics and 5 G technology, high flame retardancy and low toxicity epoxy resin have been crucial. Hence, the bio-carbon dot (CD) doped with N, P, and Mo elements was prepared by hydrothermal method using corn straw as the biomass carbon source, ethylenediamine as the nitrogen source, and phosphomolybdic acid as the phosphorus and molybdenum source. As a P-containing compound, ADP complexed with CD containing the transition metal element Mo on the surface to obtain complexes (ADP/CD). The flame retardant epoxy resin composites (EP/ADP/CD) were further prepared by ADP/CD as a flame retardant and 4,4′-diaminodiphenylmethane (DDM) as a curing substance. Transmission electron microscopy (TEM) and Fourier transform infrared spectroscopy (FTIR) were used to analyze the shape and chemical structure of CD. The experimental results indicate that when the additive amount of ADP/CD was 4 % (ADP: CD=3.5:0.5), the limiting oxygen index (LOI) of the EP/3.5ADP/0.5CD was 37.5 % (41.5 % higher than pure EP) and reached the UL94 V-0 rate. Cone calorimeter testing revealed a 51.4 %, 39.1 %, 19.6 %, and 70.4 % decrease in the peak heat release rate (pHRR), total heat release (THR), carbon monoxide production (COP), and carbon dioxide production (CO 2 P) of EP/ADP/CD. respectively, then with EP. Furthermore, the mechanical properties of EP/3.5ADP/0.5CD were discussed. Therefore, this work designs a flame-retardant carbon dot , providing a new scheme for creating a multifunctional epoxy resin with flame retardancy, smoke reduction, and toxicity reduction.
研究领域:
材料科学
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化学
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消防安全工程
✓ 已验证
产品关联
DOI
高影响因子
EXPERIMENTAL EYE RESEARCH
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2021
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IF 3.467
Lei Tao,Danxue He,Chunyan Liao,Binxiang Cai,Chao Chen,Yan Wang,Jingmeng Chen,Zuguo Liu,Yalin Wu
Retinal pigment epithelium (RPE) cell apoptosis arising from all- trans -retinal (atRAL) is in close contact with the etiology of dry age-related macular degeneration (AMD) and autosomal recessive Stargardt's disease (STGD1), but its underlying mechanisms remain elusive. In this study, we reported that c-Jun N -terminal kinase (JNK) activation facilitated atRAL-induced apoptosis of RPE cells. Reactive oxygen species production and endoplasmic reticulum stress were identified as two of major upstream events responsible for activating JNK signaling in atRAL-loaded RPE cells. Inhibiting JNK signaling rescued RPE cells from apoptosis induced by atRAL through attenuating caspase-3 activation leading to poly-ADP-ribose polymerase (PARP) cleavage, and DNA damage response . Abca4 −/− Rdh8 −/− mice upon light exposure exhibit rapidly increased accumulation of atRAL in the retina , and display severe RPE degeneration, a primary attribute of dry AMD and STGD1. Reducing JNK signaling by intraperitoneally injected JNK–IN-8 was highly effective in preventing RPE atrophy and apoptosis in light-exposed Abca4 −/− Rdh8 −/− mice. These findings afford a further understanding for contribution of JNK activation by atRAL to retinal damage .
研究领域:
眼科学
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分子生物学
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细胞生物学
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神经退行性疾病
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）