Fine particulate matter leads to reproductive impairment in male rats by overexpressing phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway

Cao, Xining; Yan, Chao; Liu, Dongyao; Peng, Jinpu; Chen, Jinjun; Zhou, Yue; Chen, Long; He, Dalin; Lin, Tao; Shen, Lianju; Wei, Guanghui

doi:10.1016/j.toxlet.2015.06.015

Cited by 74 publications

(44 citation statements)

References 76 publications

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“…This is consistent with the findings of Cao et al (2015). The results of qRT-PCR and Western blotting demonstrated that compared with the control group the expression levels of α6-integrin and β1-integrin mRNA and protein in the exposure group were significantly downregulated.…”

Section: Discussionsupporting

confidence: 90%

Gasoline exhaust damages spermatogenesis through downregulating α6-integrin andβ1-integrinin the rat model

Luo

Zhao

et al. 2018

Andrologia

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The health influence of air pollution has been an international public health concern. Increasing evidence has suggested that air pollution has been associated with decreased sperm quality. However, the underlying molecular mechanisms are still not fully elucidated. We aimed to verify whether gasoline exhaust leads to reproductive impairment by injuring spermatogonial stem cells and explore its underlying molecular mechanism. Twenty male Sprague-Dawley rats were randomly divided into two groups: the exposure group (n = 10) and the control group (n = 10). After 6-month exposure, the sperm count and morphology were determined. The histological changes in the seminiferous tubules were examined by HE staining. The expression of α6-integrin and β1-integrin was assessed with Quantitative RT-PCR, Western blot and Immunohistochemical staining. Compared with control group, male rats exposed to gasoline exhaust showed significantly reduced sperm count, increased sperm abnormality rate and the total number of spermatogonia, primary spermatocytes, secondary spermatocytes, spermatids were decreased. (all p < .01). The expression levels of α6-integrin and β1-integrin in the exposure group were significantly lower than those in the control group (all p < .01). Our study showed that exposure to gasoline exhaust caused impairment to spermatogonial stem cells through downregulating α6-integrin and β1-integrin.

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Section: Discussionsupporting

confidence: 90%

Gasoline exhaust damages spermatogenesis through downregulating α6-integrin andβ1-integrinin the rat model

Luo

Zhao

et al. 2018

Andrologia

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“…Similar investigations have been previously based on very high PM exposure rates (Li et al, 2015;Cao et al, 2015). Starting from the dose proposed for repeated instillation protocol by Li et al (2015), we reduced the cumulative dose of PM 2.5 at 1.5, 3.0, and 6.0 mg/kg BW for two weeks in this study.…”

Section: Study Protocolmentioning

confidence: 75%

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Wu¹,

Zhang²

2018

J. Toxicol. Sci.

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-Epidemiological studies have confirmed that ambient fine particulate matter (PM 2.5 ) exposure is associated with cardiovascular disease (CVD). However, the underlying mechanisms in PM 2.5 exposure-induced heart injury are largely unknown. It has been acknowledged that NADPH oxidase (Nox) 4 plays a critical role in CVD development. To investigate the acute effects of PM 2.5 on the mouse heart and the role of Nox4 in PM 2.5 exposure-induced cardiac injury, C57BL/6J mice were instilled with saline or 1.5, 3.0, 6.0 mg/kg BW PM 2.5 suspension for two weeks (five days per week). The levels of malondialdehyde (MDA), super oxide dismutase (SOD), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β in heart supernatants were determined using related kits. The expression of Nox4, p67 phox , p47 phox and p22 phox in heart tissue was evaluated by immunofluorescence staining or Western blotting, respectively. Protein levels of p53, Bax, Bcl-2 and Caspase-3 in the heart were examined using immunohistochemical staining and Western blotting. TUNEL assay was used to measure myocardial apoptosis. PM 2.5 exposure leads to obvious cardiac injury. PM 2.5 exposure increases MDA level and iNOS activity, and decreases activity of SOD in heart supernatants of mice. High levels of TNF-α and IL-1β in heart supernatants of mice with PM 2.5 instillation were determined. Nox4 and Noxassociated subunits such as p67 phox , p47 phox and p22 phox expression levels were increased in heart tissue of mice after PM 2.5 exposure. Additionally, PM 2.5 exposure causes myocardial apoptosis in the mouse heart. This study suggested that Nox4 is involved in PM 2.5 exposure-induced cardiac injury in mice.

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“…On the other hand, among the significant downregulation pathways, the TGF-β signaling pathway has been documented in particle-induced toxicity (Xie et al 2015). PM 2.5 exposure could lead to oxidative stress via the PI3K/Akt signaling pathway on male reproduction in rats (Cao et al 2015). PM 2.5 could induce oxidative stress through activating the ERK/ AKT/NF-κB signaling pathway in endothelial cells which provides new insights into the pathophysiology of cardiovascular-related diseases relating to the air pollution (Rui et al 2016).…”

Section: Discussionmentioning

confidence: 99%

Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

Lin

Yang

Asweto

et al. 2017

Environ Sci Pollut Res

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Air pollution has been a major environment-related health threat. Most of the studies on PM toxicity have verified on the cardiovascular system and endothelial cells. However, researches on PM-induced myocardial-related toxicity are limited. This study aims to fully understand the toxic effects of PM on human myocardial cell (AC16) and explore its molecular mechanism based on microarray analysis and bioinformatics analysis. Microarray data analysis manifested that PM-induced toxicity affected expression of 472 genes compared with the control group, including 166 upregulated genes and 306 downregulated genes in human myocardial (AC16) cells. GO analysis showed that cellular processes such as immune response, cell maturation, embryonic heart tube morphogenesis, cellular response to electrical stimulus, skeletal muscle tissue regeneration, and negative regulation of signal transduction were upregulated, while regulation of transcription (DNA-dependent), rhythmic process, protein destabilization apoptotic process, and innate immune response were downregulated. The pathway analysis indicates that cell signaling pathways such as cytokine-cytokine receptor interaction, NF-κB signaling pathway, chemokine signaling pathway, endocrine and other factor-regulated calcium reabsorption, HTLV-I infection, and cell adhesion molecules (CAMs) were upregulated, while the TGF-β signaling pathway was downregulated. In addition, Signal-net showed that the TUBA4A, ADRBK2, BRIX1, SMC4, EIF5B, PRMT1, ATG4B, and NDC80 genes were significantly decreased, while the expression of the KRT6B gene was markedly increased compared with the control group. All the genes were verified by qRT-PCR. This study had provided new bioinformatics evidences in PM-induced myocardial tissue toxicity which is necessary for further cardiovascular system toxicity studies.

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Fine particulate matter leads to reproductive impairment in male rats by overexpressing phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway

Cited by 74 publications

References 76 publications

Gasoline exhaust damages spermatogenesis through downregulating α6-integrin andβ1-integrinin the rat model

Gasoline exhaust damages spermatogenesis through downregulating α6-integrin andβ1-integrinin the rat model

The involvement of Nox4 in fine particulate matter exposure-induced cardiac injury in mice

Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

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