1 H NMR-based metabolomics study on repeat dose toxicity of fine particulate matter in rats after intratracheal instillation

Zhang, Yannan; Hu, Hejing; Shi, Yanfeng; Yang, Xiaozhe; Cao, Lige; Wu, Jing; Asweto, Collins Otieno; Lin, Feng; Duan, Junchao; Sun, Zhiwei

doi:10.1016/j.scitotenv.2017.02.149

Cited by 110 publications

(58 citation statements)

References 60 publications

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“…In this study, the BTB disruption could be a potential reason for PM 2.5 ‐caused reproductive dysfunction in male rat thus led to less sperm. Meanwhile, PM 2.5 is a complex compound composes of many endocrine‐disrupting chemical such as polycyclic aromatic hydrocarbons that influences the endocrine system at the hormone level, such as testicular testosterone by inhibiting 3 beta‐hydroxysteroid dehydrogenase (3β‐HSD) and steroidogenic acute regulatory protein (StAR) . Testosterone is curial for spermatogenesis and integrity of BTB .…”

Section: Discussionmentioning

confidence: 99%

“…The details of PM 2.5 extraction have been reported in previous work . A large‐volume air particle sampler (TH‐1000CII, Wuhan Tianhong, China) and quartz fiber filters (8 × 10 in, Pall) were used to collect particulate matters from April to May, 2016 in Beijing, China.…”

Section: Methodsmentioning

confidence: 99%

“…The details of PM 2.5 extraction have been reported in previous work. 21 A large-volume air particle sampler (TH-1000CII, Wuhan Tianhong, China) and quartz fiber filters (8 3 10 in, Pall) were used to collect particulate matters from April to May, 2016 in Beijing, China. After collected, each sampled filter was cut into small pieces and sonicated in ultrapure water for six 30-min cycles using ultrasonic bath sonicator.…”

Section: Pm 25 Samplesmentioning

confidence: 99%

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Fine particle matter disrupts the blood–testis barrier by activating TGF‐β3/p38 MAPK pathway and decreasing testosterone secretion in rat

Liu

Ren

Wei

et al. 2018

Environmental Toxicology

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Fine particle matter (PM) is correlated with male reproductive dysfunction in animals and humans, but the underlying mechanisms remain unknown. To investigate the toxic mechanism of PM, 32 male Sprague-Dawley (SD) rats were exposed to saline or PM with the doses of 1.8, 5.4, and 16.2 mg/kg.b.w. via intratracheal instillation, respectively, one time every 3 days, in total times for 30 days. Sperm concentration, hormone level, the expressions of BTB-associated protein and the mitogen-activated protein kinase (MAPK) pathway, tumor necrosis factor α and transforming growth factor β3 levels were detected. The results showed a decrease in sperm number, testosterone and luteinizing hormone levels and altered ultrastructure of BTB in testis of rat after exposure to PM . The protein levels of N-Cadherin, Occludin, Claudin-11, and Connexin-43 were significantly decreased in the testes. TGF-β3 content in testes showed increase, with the p-p38/p38 MAPK ratio also increasing after PM exposure. These results demonstrate that PM restrained the expressions of BTB-associated proteins through activating TGF-β3/p38 MAPK pathway and decreasing testosterone secretion, and therefore lead to the damage of BTB resulting in the decrease of sperm quality, which might be the potential reasons for its negative effects on spermatogenesis and male reproduction.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Pm 25 Samplesmentioning

confidence: 99%

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Fine particle matter disrupts the blood–testis barrier by activating TGF‐β3/p38 MAPK pathway and decreasing testosterone secretion in rat

Liu

Ren

Wei

et al. 2018

Environmental Toxicology

Self Cite

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“…After collection, the quartz fiber filters were cut into small pieces (5 × 5 mm 2 ), sonicated in ultrapure water for 180 minutes (30 min/time, 6 times), and then the solution was filtered using 8‐layer sterile gauze. Thereafter, the PM 2.5 powder was extracted using a vacuum freeze dryer and then was suspended in normal saline (NS) . PM 2.5 size was measured using dynamic light scattering (ZEN3690; Malvern Instruments Ltd, Malvern, UK), and the average diameter was ~300 nm.…”

Section: Methodsmentioning

confidence: 99%

“…Twelve male Sprague–Dawley rats (weight, 200 ± 20 g) were randomly divided into 2 groups ( n = 6) after acclimatization. Six rats were treated with the PM 2.5 solution (16.2 mg/kg body weight, twice a week) for 4 weeks, and the other rats treated with an equivalent volume (0.6 mL) of NS served as the control group . The PM 2.5 solution or NS was instilled into rat lungs by inserting a vein‐detained needle (14 G) into the trachea carefully through its rima glottidis after anesthetization, as shown in Figure C.…”

Section: Methodsmentioning

confidence: 99%

Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance

Zhang

et al. 2019

Magnetic Resonance in Med

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Purpose:To demonstrate the feasibility of 129 Xe MR in evaluating the pulmonary physiological changes caused by PM 2.5 in animal models. Methods: Six rats were treated with PM 2.5 solution (16.2 mg/kg) by intratracheal instillation twice a week for 4 weeks, and another six rats treated with normal saline served as the control cohort. Pulmonary function tests, hyperpolarized 129 Xe multi-b diffusion-weighted imaging, and chemical shift saturation recovery MR spectroscopy were performed on all rats, and the pulmonary structure and functional parameters were obtained from hyperpolarized 129 Xe MR data. Additionally, histological analysis was performed on all rats to evaluate alveolar septal thickness. Statistical analysis of all the obtained parameters was performed using unpaired 2-tailed t tests. Results: Compared with the control group, the measured exchange time constant increased from 11.74 ± 2.39 to 14.00 ± 2.84 ms (P < .05), and the septal wall thickness increased from 6.17 ± 0.48 to 6.74 ± 0.52 μm (P < .05) in the PM 2.5 cohort by 129 Xe MR spectroscopy, which correlated well with that obtained using quantitative histology (increased from 5.52 ± 0.32 to 6.20 ± 0.36 μm). Additionally, the mean TP/GAS ratio increased from 0.828 ± 0.115 to 1.019 ± 0.140 in the PM 2.5 cohort (P = .021). Conclusions: Hyperpolarized 129 Xe MR could quantify the changes in gas exchange physiology caused by PM 2.5 , indicating that the technique has the potential to be a useful tool for evaluation of pulmonary injury caused by air pollution in the future. K E Y W O R D Sair pollution, gas exchange, hyperpolarized 129 Xe, lung injury, PM 2.5 570 | ZHANG et Al.

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Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells

Nan

Sun

Yang

et al. 2023

J of Applied Toxicology

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Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL and its positive reference 50 μg/mL, respectively. The doses were respectively defined on the cell viabilities >95% (p = 0.354) and >90% (p = 0.004) when treated acutely (24 h). To mimic the long‐term exposure, AC16 was cultured from the 1st to 30th generations and treated with PM2.5 24 h in every three generations. The integration of proteomic and metabolomic analysis was applied, and 212 proteins and 172 metabolites were significantly altered during the experiments. The NOAEL PM2.5 induced both dose‐ and time‐dependent disruption, which showed the dynamic cellular proteomic response and oxidation accumulation, the main metabolomics changes were ribonucleotide, amino acid, and lipid metabolism that have involved in stressed gene expression, and starving for energy metabolism and lipid oxidation. In summary, these pathways interacted with the monotonically increasing oxidative stress and led to the accumulated damage in AC16 and implied that the safe threshold of PM2.5 may be non‐existent when a long‐term exposure occurred.

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1 H NMR-based metabolomics study on repeat dose toxicity of fine particulate matter in rats after intratracheal instillation

Cited by 110 publications

References 60 publications

Fine particle matter disrupts the blood–testis barrier by activating TGF‐β3/p38 MAPK pathway and decreasing testosterone secretion in rat

Fine particle matter disrupts the blood–testis barrier by activating TGF‐β3/p38 MAPK pathway and decreasing testosterone secretion in rat

Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells

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1 H NMR-based metabolomics study on repeat dose toxicity of fine particulate matter in rats after intratracheal instillation

Cited by 110 publications

References 60 publications

Fine particle matter disrupts the blood–testis barrier by activating TGF‐β3/p38 MAPK pathway and decreasing testosterone secretion in rat

Fine particle matter disrupts the blood–testis barrier by activating TGF‐β3/p38 MAPK pathway and decreasing testosterone secretion in rat

Quantitative evaluation of lung injury caused by PM2.5 using hyperpolarized gas magnetic resonance

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells

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Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM_2.5 induced accumulative effects in AC16 cells