Formaldehyde exposure inhibits the expression of mammalian target of rapamycin in rat testis

Fang, Jing; Li, Donghui; Yu, Xiaoqing; Lv, Mo-Qi; Bai, Lizhi; Du, Liangzhi; Zhou, Daohong

doi:10.1177/0748233715592992

Cited by 14 publications

(7 citation statements)

References 31 publications

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“…reported the downregulation of the mTOR/P70S6K1 signalling pathway after PM 2.5 exposure ( Zhang et al, 2019 ), and Fang et al . found that formaldehyde exposure inhibits the expression of mTOR in a dose-dependent manner ( Fang et al, 2015 ). Formaldehyde exposure has been reported to result in DPCs in lymphocytes, which was then shown to be reversed by the FANCD2-participating pathway ( Ren et al, 2013 ).…”

Section: Resultsmentioning

confidence: 99%

Combined exposure to formaldehyde and PM2.5: Hematopoietic toxicity and molecular mechanism in mice

Yang²,

et al. 2020

Environment International

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PM 2.5 and formaldehyde (FA) are major outdoor and indoor air pollutants in China, respectively, and both are known to be harmful to human health and to be carcinogenic. Of all the known chronic health effects, leukaemia is one of the most serious health risks associated with these two pollutants. To explore the influence and underlying mechanisms of exposure to formaldehyde and PM 2.5 on hematopoietic toxicity, we systematically studied the toxicity induced in hematopoietic organs: bone marrow (BM); spleen; and myeloid progenitor cells (MPCs). Male Balb/c mice were exposed to: PM 2.5 (20, 160 μg/kg·d) at a dose of 40 μL per mouse or formaldehyde (0.5, 3.0 mg/m 3 ) for 8 h per day for 2 weeks or co-exposed to formaldehyde and PM 2.5 (20 μg/kg·d PM 2.5 + 0.5 mg/m 3 FA, 20 μ/kg·d PM 2.5 + 3 mg/m 3 FA, 160 μg/kg·d PM 2.5 + 0.5 mg/m 3 FA, 160 μg/kg·d PM 2.5 + 3 mg/m 3 FA) for 2 weeks. Similar toxic effects were found in the formaldehyde-only and PM 2.5 -only groups, including significant decrease of blood cells and MPCs, along with decreased expression of hematopoietic growth factors. In addition, individual exposure of formaldehyde or PM 2.5 increased oxidative stress, DNA damage and immune system disorder by destroying the balance of Th1/Th2, and Treg/Th17. DNA repair was markedly inhibited by deregulating the mammalian target of rapamycin (mTOR) pathway. Combined exposure to PM 2.5 and formaldehyde led to more severe effects. Administration of Vitamin E (VE) was shown to attenuate these effects. In conclusion, our findings suggested that PM 2.5 and formaldehyde may induce hematopoietic toxicity by reducing the expression of hematopoietic growth factors, increasing oxidative stress and DNA damage, activating the ‘immune imbalance’ pathway and suppressing the DNA-repair related mTOR pathway. The hematopoietic toxicity induced by combined exposure of PM 2.5 and formaldehyde might provide further insights into the increased incidence of hematological diseases, including human myeloid leukaemia.

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Section: Resultsmentioning

confidence: 99%

Combined exposure to formaldehyde and PM2.5: Hematopoietic toxicity and molecular mechanism in mice

Yang²,

et al. 2020

Environment International

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“…Spermatogenesis, the transformation of spermatogonia into sperm, is a well-orchestrated and precisely-regulated biological process which is strictly regulated by phase-specific gene expression [4, 29–31]. Noncoding RNAs such as microRNAs (miRNAs), PIWI-interacting RNAs (piRNAs) and long non-coding RNAs (lncRNAs) are important post-transcriptional regulators of gene expression in multiple stages of spermatogenesis [32, 33].…”

Section: Discussionmentioning

confidence: 99%

CircRNA expression profile and functional analysis in testicular tissue of patients with non-obstructive azoospermia

Zhang

Zhou

et al. 2019

Reprod Biol Endocrinol

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BackgroundNon-obstructive azoospermia (NOA) is a multifactorial disorder whose molecular basis remains largely unknown. Circular RNAs (CircRNAs), a novel class of endogenous RNAs, have been recognized to play important roles in many biological processes. However, little is known about the expression patterns and functions of circRNAs in human testes involved in NOA.MethodsIn this study, the testicular circRNA expression profile were explored in NOA patients and the controls by high-throughput circRNA microarray. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to confirm the microarray data. Bioinformatics analyses including the circRNA/miRNA/mRNA interaction network, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were used to predict the functions of differentially expressed circRNAs.ResultsA total of 368 differentially down-regulated and 526 up-regulated circRNAs were detected in NOA patients. These findings have been verified by qRT-PCR on 6 selected circRNAs. Among these differentially expressed circRNAs, the hsa_circRNA_0023313 was obviously up-regulated in testicular tissue of NOA patients. The most likely potential target miRNA for hsa_circRNA_0023313 include hsa-miR-520d-3p, hsa-miR-373-3p, hsa-miR-372-3p, hsa-miR-302c-3p and hsa-miR-130b-5p. Function analysis indicated that hsa_circRNA_0023313 was ubiquitin-protein transferase activity and chromatin binding. KEGG analysis revealed that the top five pathways related to hsa_circRNA_0023313 were endocytosis, meiosis, FoxO signaling pathway, ubiquitin mediated proteolysis and AMPK signaling pathway.ConclusionsThis is the first report that the testicular circRNA expression profile is altered in NOA patients indicating circRNAs might play important roles in regulating spermatogenesis and be potential biomarkers for the diagnosis and treatment of NOA.

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“…It is a colorless, highly water soluble, and reactive substance that could rapidly diffuse into many organs and tissues (Tang et al, 2009). Currently, despite many preventive measures taken to reduce FA contaminant, exposure to FA remains one of the most prominent environmental health problems worldwide (Duong et al, 2011; Fang et al, 2016; Han et al, 2015; Tang et al, 2009; Zhou et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Formaldehyde inhalation triggers autophagy in rat lung tissues

Liu

Zhou

et al. 2018

Toxicol Ind Health

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Formaldehyde (FA), a ubiquitous environmental contaminant, has long been suspected of causing lung injury. However, the molecular and cellular mechanisms underlying this phenomenon remain elusive. The aim of this study was to elucidate the role of autophagy in lung injury induced by FA inhalation. In this study, lung weight coefficient, interleukin 8 in bronchoalveolar fluid, and histopathological examination were used to evaluate the lung injury. Moreover, electron microscopy, Western blotting for the ratio of LC3-II/LC3-I were used to detect autophagy in lung tissues. Our results indicated that the lung toxicity of FA inhalation is dose dependent. Lung weight coefficient, inflammatory response, and histopathological structure in the 0.5 mg/m 3 FA exposure group showed no obvious changes compared with the control. However, exposure to 5 and 10 mg/m 3 FA produced lung injury including pulmonary edema, histological changes, and inflammatory responses. Furthermore, the alterations of autophagy correlated with lung injury. Taken together, these data indicate that FA exposure triggers autophagy of alveolar epithelial cells, which might play a pivotal role in lung injury.

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Formaldehyde exposure inhibits the expression of mammalian target of rapamycin in rat testis

Cited by 14 publications

References 31 publications

Combined exposure to formaldehyde and PM2.5: Hematopoietic toxicity and molecular mechanism in mice

Combined exposure to formaldehyde and PM2.5: Hematopoietic toxicity and molecular mechanism in mice

CircRNA expression profile and functional analysis in testicular tissue of patients with non-obstructive azoospermia

Formaldehyde inhalation triggers autophagy in rat lung tissues

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