Asian Pacific Journal of Cancer Prevention

Asian Pacific Journal of Cancer Prevention (아시아태평양암예방학회)
권호 표지
DOI QR코드

DOI QR Code

Inhaled Formaldehyde Induces Bone Marrow Toxicity via Oxidative Stress in Exposed Mice

  • Published : 2014.07.15
Download PDF
⟨ Previous Next ⟩

Abstract

Formaldehyde (FA) is an economically important chemical, and has been found to cause various types of toxic damage to the body. Formaldehyde-induced toxic damage involves reactive oxygen species (ROS) that trigger subsequent toxic effects and inflammatory responses, which may increase risk of cancer. Therefore, in the present study, we aimed to investigate the possible toxic mechanism in bone marrow caused by formaldehyde. In accordance with the principle of randomization, the mice were divided into four groups of 6 mice per group. One group was exposed to ambient air and the other three groups were exposed to different concentrations of formaldehyde (20, 40, $80mg/m^3$) for 15 days in the respective inhalation chambers, 2h a day. At the end of the 15-day experimental period, all mice were killed. Bone marrow cells were obtained. Some of those were used for the determination of blood cell numbers, bone marrow karyote numbers, CFU-F, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content; others were used for the determination of mitochondrial membrane potential (MMP), cell cycle and Bcl-2, Bax, CytC protein expression. WBC and PLT numbers in median and high dose groups were obvious reduced, but there was no change on RBC numbers. There was also reduced numbers of bone marrow karyotes and CFU-F in the high dose group. SOD activity was decreased, but MDA content was increased. MMP and Bcl-2 expression were decreased with increasing formaldehyde concentration, while expression of Bax and Cyt C was increased. We also observed change in cell cycling, and found that there was S phase arrest in the high dose group. Our study suggested that a certain concentration of formaldehyde could have toxic effects on the hematopoietic system, with oxidative stress as a critical effect.

Keywords

References

  1. Akan Z, Garip AI (2013). Antioxidants may protect cancer cells from apoptosis signals and enhance cell viability. Asian Pac J Cancer Prev, 14, 4611-14. https://doi.org/10.7314/APJCP.2013.14.8.4611
  2. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans (2012). A Review of Human Carcinogens: Chemical Agents and Related Occupations. WHO International Agency for Research on Cancer, 100, 401-35.
  3. Klaunig JE, Wang Z, Pu X, et al (2011). Oxidative stress and oxidative damage in chemical carcinogenesis. Toxicol Appl Pharmacol, 254, 86-99. https://doi.org/10.1016/j.taap.2009.11.028
  4. Kong CZ, Zhang Z (2013). Bcl-2 overexpression inhibits generation of intracellular reactive oxygen species and blocks adriamycin-induced apoptosis in bladder cancer cells. Asian Pac J Cancer Prev, 14, 895-901 https://doi.org/10.7314/APJCP.2013.14.2.895
  5. Kryston TB, Georgiev AB, Pissis P, et al (2011). Role of oxidative stress and DNA damage in human carcinogenesis. Mutat Res, 711, 193-201. https://doi.org/10.1016/j.mrfmmm.2010.12.016
  6. Matsuoka T, Takaki A, Ohtaki H, et al (2010). Early changes to oxidative stress levels following exposure to formaldehyde in ICR mice. J Toxicol Sci, 35, 721-30. https://doi.org/10.2131/jts.35.721
  7. NTP (National Toxicology Program) (2011). Report on Carcinogens, Twelfth Edition. Research Triangle Park, 195-205.
  8. Ola MS, Nawaz M, Ahsan H (2011). Role of Bcl-2 family proteins and caspases in the regulation of apoptosis. Mol Cell Biochem, 351, 41-58. https://doi.org/10.1007/s11010-010-0709-x
  9. Park KJ, Kim YJ, Kim J, et al (2012). Protective Effects of Peroxiredoxin on Hydrogen Peroxide Induced Oxidative Stress and Apoptosis in Cardiomyocytes. Korean Circulation Journal, 42, 23-32. https://doi.org/10.4070/kcj.2012.42.1.23
  10. Renstrom J, Kroger M, Peschel C, et al (2010). How the niche regulates hematopoietic stem cells. Chem Biol Interact, 184, 7-15. https://doi.org/10.1016/j.cbi.2009.11.012
  11. Wong VC, Cash HL, Morse JL, et al (2012). S-phase sensing of DNA-protein crosslinks triggers TopBP1-independent ATR activation and p53-mediated cell death by formaldehyde. Cell Cycle, 11, 2526-37. https://doi.org/10.4161/cc.20905
  12. Zhang YC, Liu XD, McHale C, et al (2013). Bone marrow injury induced via oxidative stress in mice by inhalation exposure to formaldehyde. PloS one, 8, 1-10.
  13. Zhou DX, Qiu SD, Zhang J, et al (2006). The protective effect of vitamin E against oxidative damage caused by formaldehyde in the testes of adult rats. Asian J Androl, 8, 584-88. https://doi.org/10.1111/j.1745-7262.2006.00198.x

Cited by

  1. Antioxidant-mediated preventative effect of Dragon-pearl tea crude polyphenol extract on reserpine-induced gastric ulcers vol.10, pp.1, 2015, https://doi.org/10.3892/etm.2015.2473
  2. Evaluation of oxidative stress markers in the heart and liver of rainbow trout (Oncorhynchus mykiss walbaum) exposed to the formalin vol.42, pp.6, 2016, https://doi.org/10.1007/s10695-016-0260-0
  3. Do chromosome changes in blood cells implicate formaldehyde as a leukemogen? vol.47, pp.2, 2017, https://doi.org/10.1080/10408444.2016.1211987
  4. Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment vol.91, pp.1, 2017, https://doi.org/10.1007/s00204-016-1733-8
  5. Formaldehyde-induced neurotoxicity in rat cerebellar cortex and possible protective effects of fatty acids from omega 3 and wheat germ oil supplement: a histopathological and biochemical study pp.2046-0236, 2018, https://doi.org/10.1080/01478885.2018.1458176