Chronic exposure to diesel exhaust particulate matter impairs meiotic progression during spermatogenesis in a mouse model

Yang, Wei; Xu, Yanyi; Pan, Hongjie; Tian, Fang; Wang, Yuzhu; Mao, Xia; Hu, Jun; Yang, Mingjun; Tao, Shimin; Sun, Shenfei; Kan, Haidong; R, Li; Zhao, Ying; Li, Weihua

doi:10.1016/j.ecoenv.2020.110881

Cited by 15 publications

(12 citation statements)

References 27 publications

(51 reference statements)

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“…The connection between VC and spermatogenic dysfunction is still controversial. LncRNAs play various functions in many diseases through signalling pathways 22,23 . Previous studies have shown that lncRNAs play roles in VC‐related male infertility through the regulation of hypoxia responses 23 .…”

Section: Discussionmentioning

confidence: 99%

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Long noncoding RNAs regulated spermatogenesis in varicocele‐induced spermatogenic dysfunction

et al. 2022

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Objectives:To evaluate the expression, potential functions and mechanisms of long noncoding RNAs (lncRNAs) in the pathogenesis of varicocele (VC)-induced spermatogenic dysfunction. Materials and Methods:We established a rat model with left experimental VC and divided rats into the sham group, the VC group, and the surgical treatment group (each group, n = 10). Haematoxylin and eosin (HE) staining and sperm quality were analysed to evaluate spermatogenesis function. LncRNA expression profiles were analysed using lncRNA-Seq (each group n = 3) and validated using quantitative realtime polymerase chain reaction (each group n = 10). Correlation analysis and gene target miRNA prediction were used to construct competing endogenous RNA network.The regulated signalling pathway and spermatogenic dysfunction of differentially expressed lncRNAs (DE lncRNAs) were validated by Western blot.Results: HE detection and sperm quality analysis showed that VC could induce spermatogenic dysfunction. Eight lncRNAs were upregulated and three lncRNAs were downregulated in the VC group compared with the sham group and surgical treatment group. The lncRNA of NONRATG002949.

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Section: Discussionmentioning

confidence: 99%

“…LncRNAs play various functions in many diseases through signalling pathways. 22,23 Previous studies have shown that lncRNAs play roles in VC-related male infertility through the regulation of hypoxia responses. 23 Although a large number of lncRNAs have been found in the testis, their biological function remains to be…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNAs regulated spermatogenesis in varicocele‐induced spermatogenic dysfunction

et al. 2022

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“… 43 , 44 GnRh is associated with sperm generation and smooth progression of meiosis. 45 , 46 Therefore, we measured the levels of GnRh, LH and testosterone. We found that PSE-NPs could increase the level of GnRh, LH and testosterone significantly.…”

Section: Discussionmentioning

confidence: 99%

“…If the GnRhR signaling pathway is inhibited, then expression of genes related to meiosis is also inhibited, thereby which reduces sperm production. 45 , 51 SCP3 is a key factor in meiosis, expressed mainly in primary spermatocytes. 52 SCP3-knockout homozygous male mice are infertile, with a significant decrease in the Testes Index and many apoptotic sperm cells.…”

Section: Discussionmentioning

confidence: 99%

Pseudoephedrine Nanoparticles Alleviate Adriamycin-Induced Reproductive Toxicity Through the GnRhR Signaling Pathway

Yuan

Zheng

et al. 2022

IJN

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Purpose Pseudoephedrine (PSE) has rapid absorption and metabolism, which limits its pharmacologic actions. We postulated that pseudoephedrine nanoparticles (PSE-NPs) with high bioavailability could overcome this limitation. The defensive function of PSE-NPs nanoparticles against adriamycin-induced reproductive toxicity in mice was studied. Methods We encapsulated PSE in polylactide-polyglycolide nanoparticles (PLGA-NPs) and verified their protective activity against testicular injury in vivo and in vitro. Results We report a promising delivery system that loads PSE into PLGA-NPs and finally assembles it into a nanocomposite particle. In vitro, PSE-NPs reduced the adriamycin-induced apoptosis of GC-1 cells significantly, improved mitochondrial energy metabolism and promoted expression of the proteins related to the gonadotropin-releasing hormone (GnRh) receptor signaling pathway. In vivo, evaluation of sperm indices and histology showed that adriamycin could induce testicular toxicity. PSE-NPs significantly increased the sperm motility of mice, reduced the percent apoptosis and oxidative stress of testes, increased serum levels of GnRh, activated the GnRhR signaling pathway in testes and promoted expression of meiosis-related factors. Conclusion In view of their safety and efficiency, these PSE-NPs have potential applications in alleviating adriamycin-induced reproductive toxicity.

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“…Besides the epidemiological evidence, several toxicological studies in animals revealed decreased male reproductive capacity caused by PM 2.5 . After PM 2.5 exposure via intratracheal instillation, injury of testicular tissue and reduced testosterone were occurred, the integrity of blood-testis barrier was destroyed, and finally sperm quality was significantly decreased (11)(12)(13). Up to now, the mechanisms of reproductive toxicity induced by PM 2.5 mainly focused on ROS generation, DNA damage, mitochondrial dysfunction and the disturbance of hypothalamic-pituitary-gonadal (HPG) axis.…”

Section: Introductionmentioning

confidence: 99%

Analysis by Metabolomics and Transcriptomics for the Energy Metabolism Disorder and the Aryl Hydrocarbon Receptor Activation in Male Reproduction of Mice and GC-2spd Cells Exposed to PM2.5

et al. 2022

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Fine particulate matter (PM2.5)-induced male reproductive toxicity arouses global public health concerns. However, the mechanisms of toxicity remain unclear. This study aimed to further investigate toxicity pathways by exposure to PM2.5in vitro and in vivo through the application of metabolomics and transcriptomics. In vitro, spermatocyte-derived GC-2spd cells were treated with 0, 25, 50, 100 μg/mL PM2.5 for 48 h. In vivo, the real-world exposure of PM2.5 for mouse was established. Forty-five male C57BL/6 mice were exposed to filtered air, unfiltered air, and concentrated ambient PM2.5 in Tangshan of China for 8 weeks, respectively. The results in vitro and in vivo showed that PM2.5 exposure inhibited GC-2spd cell proliferation and reduced sperm motility. Mitochondrial damage was observed after PM2.5 treatment. Increased Humanin and MOTS-c levels and decreased mitochondrial respiratory indicated that mitochondrial function was disturbed. Furthermore, nontargeted metabolomics analysis revealed that PM2.5 exposure could disturb the citrate cycle (TCA cycle) and reduce amino acids and nucleotide synthesis. Mechanically, the aryl hydrocarbon receptor (AhR) pathway was activated after exposure to PM2.5, with a significant increase in CYP1A1 expression. Further studies showed that PM2.5 exposure significantly increased both intracellular and mitochondrial reactive oxygen species (ROS) and activated NRF2 antioxidative pathway. With the RNA-sequencing technique, the differentially expressed genes induced by PM2.5 exposure were mainly enriched in the metabolism of xenobiotics by the cytochrome P450 pathway, of which Cyp1a1 was the most significantly changed gene. Our findings demonstrated that PM2.5 exposure could induce spermatocyte damage and energy metabolism disorder. The activation of the aryl hydrocarbon receptor might be involved in the mechanism of male reproductive toxicity.

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Chronic exposure to diesel exhaust particulate matter impairs meiotic progression during spermatogenesis in a mouse model

Cited by 15 publications

References 27 publications

Long noncoding RNAs regulated spermatogenesis in varicocele‐induced spermatogenic dysfunction

Long noncoding RNAs regulated spermatogenesis in varicocele‐induced spermatogenic dysfunction

Pseudoephedrine Nanoparticles Alleviate Adriamycin-Induced Reproductive Toxicity Through the GnRhR Signaling Pathway

Analysis by Metabolomics and Transcriptomics for the Energy Metabolism Disorder and the Aryl Hydrocarbon Receptor Activation in Male Reproduction of Mice and GC-2spd Cells Exposed to PM2.5

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