Early oxidative stress, DNA damage and inflammation resulting from subcutaneous injection of sulfur mustard into mice

Zhang, Xiaorui; Mei, Yizhou; Wang, Tongxing; Liu, Feng; Jiang, Ning; Zhou, Wenxia; Zhang, Yongxiang

doi:10.1016/j.etap.2017.06.016

Cited by 15 publications

(15 citation statements)

References 31 publications

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“…These results suggested that the exposure to La 2 O 3 NPs might cause oxidative stress in mouse testes. Toxicity of nanoparticles is manifested by inflammation resulting from oxidative stress (Zhang et al, 2017b). NPs and MPs by intragastric administration for 60 days.…”

Section: Discussionmentioning

confidence: 99%

Effects of intragastric administration of La2O3 nanoparticles on mouse testes

et al. 2020

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Lanthanum oxide (La 2 O 3) nanoparticles (NPs) have been widely used in photoelectric and catalytic applications. However, their exposure and reproductive toxicity is unknown. In this study, the effect of the intragastric administration of two different-sized La 2 O 3 particles in the testes of mice for 60 days was investigated. Although the body weight of mice treated or not treated with La 2 O 3 NPs was not different and La 2 O 3 NPs were distributed in the organs including the testis, liver, kidney, spleen, heart and brain. La 2 O 3 NPs accumulate more than micro-sized La 2 O 3 (MPs) in mice testes. The histopathological evaluation showed that moderate reproductive toxicity induced by La 2 O 3 NPs in the testicle tissues. Furthermore, increased MDA, 8-OHdG levels and decreased SOD activities were detected in the La 2 O 3 NP-treated groups. Moreover, qRT-PCR and western blotting data indicated that La 2 O 3 NPs affecting the blood-testis barrier (BTB)-related genes in mice testes. Taken together, these findings suggested that La 2 O 3 NPs activated inflammation responses and cross the BTB in the murine testes. This study provided useful information for risk analysis and regulation of La 2 O 3 NPs by administrative agencies.

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Section: Discussionmentioning

confidence: 99%

Effects of intragastric administration of La2O3 nanoparticles on mouse testes

et al. 2020

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“…γ-H2A.X is H2A.X (a specialized histone H2A variant) phosphorylated at Ser 139 via ATM serine/threonine kinase and ATR serine/threonine kinase (39). γ-H2A.X is widely considered as a marker of DNA damage (40,41). The results of the present study demonstrated that Ad-hTK1/hTIMP1 significantly decreased γ-H2A.X expression in H/R-treated CMVECs, indicating reduced DNA damage in H/R-treated CMVECs following transfection with Ad-hTK1/hTIMP1, which may be attributed to decreased oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Co‑expression of tissue kallikrein 1 and tissue inhibitor of matrix metalloproteinase 1 improves myocardial ischemia‑reperfusion injury by promoting angiogenesis and inhibiting oxidative stress

Huang

Chen²,

et al. 2020

Mol Med Rep

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“…However, AP18 was insufficient to completely prevent HSPA6 induction in our experiments indicating that TRPA1 is not exclusively responsible for HSPA6 up-regulation. In addition to TRPA1-mediated ROS formation, SM-induced depletion of antioxidants, lipid oxidation or direct effects on mitochondria can cause severe oxidative stress which is independent of TRPA1 and may also trigger HSPA6 expression [ 66 , 67 , 68 ].…”

Section: Discussionmentioning

confidence: 99%

Transient Receptor Potential Channel A1 (TRPA1) Regulates Sulfur Mustard-Induced Expression of Heat Shock 70 kDa Protein 6 (HSPA6) In Vitro

Lüling

John

Gudermann

et al. 2018

Cells

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The chemosensory transient receptor potential ankyrin 1 (TRPA1) ion channel perceives different sensory stimuli. It also interacts with reactive exogenous compounds including the chemical warfare agent sulfur mustard (SM). Activation of TRPA1 by SM results in elevation of intracellular calcium levels but the cellular consequences are not understood so far. In the present study we analyzed SM-induced and TRPA1-mediated effects in human TRPA1-overexpressing HEK cells (HEKA1) and human lung epithelial cells (A549) that endogenously exhibit TRPA1. The specific TRPA1 inhibitor AP18 was used to distinguish between SM-induced and TRPA1-mediated or TRPA1-independent effects. Cells were exposed to 600 µM SM and proteome changes were investigated 24 h afterwards by 2D gel electrophoresis. Protein spots with differential staining levels were analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and nano liquid chromatography electrospray ionization tandem mass spectrometry. Results were verified by RT-qPCR experiments in both HEKA1 or A549 cells. Heat shock 70 kDa protein 6 (HSPA6) was identified as an SM-induced and TRPA1-mediated protein. AP18 pre-treatment diminished the up-regulation. RT-qPCR measurements verified these results and further revealed a time-dependent regulation. Our results demonstrate that SM-mediated activation of TRPA1 influences the protein expression and confirm the important role of TRPA1 ion channels in the molecular toxicology of SM.

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Early oxidative stress, DNA damage and inflammation resulting from subcutaneous injection of sulfur mustard into mice

Cited by 15 publications

References 31 publications

Effects of intragastric administration of La<sub>2</sub>O<sub>3</sub> nanoparticles on mouse testes

Effects of intragastric administration of La<sub>2</sub>O<sub>3</sub> nanoparticles on mouse testes

Co‑expression of tissue kallikrein 1 and tissue inhibitor of matrix metalloproteinase 1 improves myocardial ischemia‑reperfusion injury by promoting angiogenesis and inhibiting oxidative stress

Transient Receptor Potential Channel A1 (TRPA1) Regulates Sulfur Mustard-Induced Expression of Heat Shock 70 kDa Protein 6 (HSPA6) In Vitro

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