Study On The Genotoxicity And Immunotoxicity Of Formaldehyde In Mice

In recent years, with the rapid development of economy, indoor fitment is growing quickly and becomes common. But what followed is the indoor pollution induced by upholstery. Formaldehyde has become one of the most important and serious indoor air pollutants for its characteristics of extensive sources, serious toxicity, high level pollution and long-term duration. Now the research of the toxicity of formaldehyde is a hot and difficult spot in the field of hygienical. This research is to explore the genotoxicity and immunotoxicity of formaldehyde in mice, which is of great significance to understand the toxicity of formaldehyde comprehensively and systematically. The research also can provide scientific basis to further evaluate the quality of indoor air and to establish a safe standard of environmental and occupational formaldehyde concentration. In this study mice were used to explore the genotoxicity and immunotoxicity of formaldehyde and the possible molecular mechanism via the method of SDS-KC1 assay and RT-PCR.The results:1.DNA-protein crosslinks induced by formaldehydeThere are a certain amount of DNA-protein crosslinks (DPC) in normal cells, which has normal connection between DNA and nuclein. Therefore, DPC is important to support the cell growth. Excessive DPC can be induced by environmental pollutants and carcinogen. Compared with other types of DNA damage, DPC is hard to be repaired, and DPC only can be in the single strand DNA, which shows that DPC can be induced during replication and transcription. So DPC has serious influence to DNA configuration and functions and can cause some important genes loss (such as tumor suppressor gene). Excessive DPC is a pathological phenomenon and a serious genetic damage in DNA.In this study, mice liver cells and the cell line of HepG2 were used to detect the formaldehyde-induced DPC by the SDS-KC1 assay. The results showed that a higher concentration of formaldehyde can induce DPC in mice liver cells and HepG2 cells.2.The repair of DPC induced by formaldehydeMany researches found that formaldehyde-induced DPC in cells can be repaired. In this study, mice liver cells and the cell line of HepG2 were used to detect the repairs of formaldehyde-induced DPC by the SDS-KC1 assay. The results indicated that formaldehyde-induced formaldehyde DPC can be markedly repaired. The DPC induced by gaseous formaldehyde mostly can be repaired in 12 h and recover to the normal level of the cells in 24h. The DPC induced by liquid formaldehyde could be repaired in 24 h.3. Immunotoxicity caused by formaldehyde in miceWHO defined asthma as a lifelong disease, asthma caused tremendous financial burden to the world. In recent 40 years, asthmatic morbidity and mortality increased continuously all the world. The gaseous pollutants were suspected to be a major reason, but the molecular mechanism of allergic asthma is not clear. So the molecular mechanisms of asthma are important to be revealed for its significance to the field of scientific research and the society.Friend et al first identified TSLP in thymic stromal cell line in 1994. Thymic stromal lymphopoietin (TSLP) is a novel IL-7-like cytokine. The symptoms of asthma could aggravate when TSLP expression was increased in the lungs of mice. Many findings suggested that TSLP represents a master switch of asthma.IL-4 plays an important role in asthma. Asthma is closely related with the increase of concentrations of IL-4. The concentrations of IL-4 will change at the different stages of disease. So the levels of IL-4 in broncho alveolar lavage fluid in the mice induced by formaldehyde can be an important indicator for the monitoring and diagnosing of asthma.The results indicated that the Tslp mRNA expression levels at 3.0 mg/m3 groups were significantly (P<0.05) higher than that in 0 mg/m~3 group, and the IL-4 levels at 1.0 mg/m~3, 3.0 mg/m~3 formaldehyde inhaled groups were significantly higher than that in 0 mg/m~3 (p<0.05), which indicated that formaldehyde might cause the disease of asthma via the path of TSLP.