Changes to Oxidative Stress Levels Following Exposure to Formaldehyde in Lymphocytes
Formaldehyde is the illegal chemical substance used
for food preservation in fish and vegetable. It can promote
carcinogenesis. Superoxide dismutases are the important
antioxidative enzymes that catalyze the dismutation of superoxide
anion into oxygen and hydrogen peroxide. The resultant level of
oxidative stress in formaldehyde-treated lymphocytes was
investigated. The formaldehyde concentrations of 0, 20, 40, 60, 80
and 120μmol/L were treated in human lymphocytes for 12 hours.
After 12 treated hours, the superoxide dismutase activity change was
measured in formaldehyde-treated lymphocytes. The results showed
that the formaldehyde concentrations of 60, 80 and 120μmol/L
significantly decreased superoxide dismutase activities in
lymphocytes (P < 0.05). The change of superoxide dismutase
activity in formaldehyde-treated lymphocytes may be the biomarker
for detect cellular injury, such as damage to DNA, due to
formaldehyde exposure.
<p>[1] IARC, “IARC Monographs on the Evaluation of Carcinogenic Risks to
Humans: Wood Dust and Formaldehyde.” IARC Scientific Publication.
No. 62, IARC, Lyon, 1995.
[2] H. Kuo, G. Jian, C. Chen, C. Liu and J. Lai, “White blood cell count as
an indicator of formaldehyde exposure.” Bull Environ Contam Toxicol.,
vol. 59, pp. 261– 267,1997.
[3] G. Speit, S. Petra and M. Oliver, “Induction and repair of formaldehydeinduced
DNA-protein crosslinks in repair-deficient human cell lines.”
Mutagenesis, vol.15, no.1, pp.85-90, 2000.
[4] B. Halliwell, “Antioxidant and human disease: a general introduction.”
Nutr.Rev., vol.55, pp. S44-S52, 1997.
[5] M. Valko, D. Leibfritz, J. Moncol, M. Cronin, M. Mazur and J. Telse R,
“Free radicals and antioxidants in normal physiological functions and
human disease.” Int. J. Biochem. Cell. Biol., vol. 39, no. 1, pp. 44–84,
2007.
[6] M. Casanova, K. T. Morgan, W. H. Steinhagen, J. I. Everitt, J. A. Popp J
A and H. d’A Heck, “Covalent binding of inhaled formaldehyde to DNA
in the respiratory tract of rhesus monkeys : pharmacokinetics, rat-tomonkey
interspecies scaling and extrapolation to man,” Fundam. Appl.
Toxicol., vol. 17, pp.409-428, 1991.
[7] M. Casanova, K.T. Morgan, E.A. Gross, O.R. Moss and HD’A Heck,
“DNA- protein-cross-links and cell replication at specific sites in the
nose of rats exposed subchronically to formaldehyde.” Fundam. Appl.
Toxicol., vol.23, pp.525-536, 1994.
[8] R.B. Conolly and M.E. Anderson, “An approach to mechanism-based
cancer risk assessment for formaldehyde.” Environ. Health. Perspect.,
vol. 101, pp.169-176, 1993.
[9] H.A. Aly, O. Domenech and A. B. Abdelnaim, “Aroclor 1254 impairs
spermatogenesis and induces oxidative stress in rat testicular
mitochondria.” Food and Chemical Toxicology., vol. 47, no.8, pp. 1733–
1738, 2009.
[10] M.D. Kadiisaka and R.P. Mason, “Acute methanol intoxication
generates free radicals in rats: an ESR spin trapping investigation .” Free
Radic. Biol. Med., vol.28, pp. 1106-1114, 2000.
[11] Y. Nakabeppu , K. Sakumi, K. Sakamoto , D. Tsuchimoto, T. Tsuzuki
and Y. Nakatsu, “Mutagenesis and carcinogenesis caused by the
oxidation of nucleic acids.” Biol. Chem., vol. 387, no. 4, pp. 373–379,
2006.
[12] D. C. Arikan, V. Bakan, E. B. Kurutas, H. Sayar and A. Coskun,
“Protective effects of tadalafil on ischemia/reperfusion injury of rat
ovary.” Journal of Pediatric Surgery. vol. 45, no. 11, pp. 2203–2209,
2010.
[13] J. Fujii, Y. Luchi, S. Matsuki and T. Ishii, “Cooperative function of
antioxidant and redox systems against oxidative stress in male
reproductive tissue.” Asian Journal of Andrology. vol.5, no.3, pp. 231-
242, 2003.
[14] K. Doreswamy, B. Shrilatha, T. Rajeshkumar and Muralidhara, “Nickelinduced
oxidative stress in testes of mice: evidence of DNA damage and
genotoxic effects.” Journal of Andrology. vol.25, no. 6, pp. 996–1003,
2004.</p>
<p>[1] IARC, “IARC Monographs on the Evaluation of Carcinogenic Risks to
Humans: Wood Dust and Formaldehyde.” IARC Scientific Publication.
No. 62, IARC, Lyon, 1995.
[2] H. Kuo, G. Jian, C. Chen, C. Liu and J. Lai, “White blood cell count as
an indicator of formaldehyde exposure.” Bull Environ Contam Toxicol.,
vol. 59, pp. 261– 267,1997.
[3] G. Speit, S. Petra and M. Oliver, “Induction and repair of formaldehydeinduced
DNA-protein crosslinks in repair-deficient human cell lines.”
Mutagenesis, vol.15, no.1, pp.85-90, 2000.
[4] B. Halliwell, “Antioxidant and human disease: a general introduction.”
Nutr.Rev., vol.55, pp. S44-S52, 1997.
[5] M. Valko, D. Leibfritz, J. Moncol, M. Cronin, M. Mazur and J. Telse R,
“Free radicals and antioxidants in normal physiological functions and
human disease.” Int. J. Biochem. Cell. Biol., vol. 39, no. 1, pp. 44–84,
2007.
[6] M. Casanova, K. T. Morgan, W. H. Steinhagen, J. I. Everitt, J. A. Popp J
A and H. d’A Heck, “Covalent binding of inhaled formaldehyde to DNA
in the respiratory tract of rhesus monkeys : pharmacokinetics, rat-tomonkey
interspecies scaling and extrapolation to man,” Fundam. Appl.
Toxicol., vol. 17, pp.409-428, 1991.
[7] M. Casanova, K.T. Morgan, E.A. Gross, O.R. Moss and HD’A Heck,
“DNA- protein-cross-links and cell replication at specific sites in the
nose of rats exposed subchronically to formaldehyde.” Fundam. Appl.
Toxicol., vol.23, pp.525-536, 1994.
[8] R.B. Conolly and M.E. Anderson, “An approach to mechanism-based
cancer risk assessment for formaldehyde.” Environ. Health. Perspect.,
vol. 101, pp.169-176, 1993.
[9] H.A. Aly, O. Domenech and A. B. Abdelnaim, “Aroclor 1254 impairs
spermatogenesis and induces oxidative stress in rat testicular
mitochondria.” Food and Chemical Toxicology., vol. 47, no.8, pp. 1733–
1738, 2009.
[10] M.D. Kadiisaka and R.P. Mason, “Acute methanol intoxication
generates free radicals in rats: an ESR spin trapping investigation .” Free
Radic. Biol. Med., vol.28, pp. 1106-1114, 2000.
[11] Y. Nakabeppu , K. Sakumi, K. Sakamoto , D. Tsuchimoto, T. Tsuzuki
and Y. Nakatsu, “Mutagenesis and carcinogenesis caused by the
oxidation of nucleic acids.” Biol. Chem., vol. 387, no. 4, pp. 373–379,
2006.
[12] D. C. Arikan, V. Bakan, E. B. Kurutas, H. Sayar and A. Coskun,
“Protective effects of tadalafil on ischemia/reperfusion injury of rat
ovary.” Journal of Pediatric Surgery. vol. 45, no. 11, pp. 2203–2209,
2010.
[13] J. Fujii, Y. Luchi, S. Matsuki and T. Ishii, “Cooperative function of
antioxidant and redox systems against oxidative stress in male
reproductive tissue.” Asian Journal of Andrology. vol.5, no.3, pp. 231-
242, 2003.
[14] K. Doreswamy, B. Shrilatha, T. Rajeshkumar and Muralidhara, “Nickelinduced
oxidative stress in testes of mice: evidence of DNA damage and
genotoxic effects.” Journal of Andrology. vol.25, no. 6, pp. 996–1003,
2004.</p>
@article{"International Journal of Biological, Life and Agricultural Sciences:58919", author = "Malinee Pongsavee", title = "Changes to Oxidative Stress Levels Following Exposure to Formaldehyde in Lymphocytes", abstract = "Formaldehyde is the illegal chemical substance used
for food preservation in fish and vegetable. It can promote
carcinogenesis. Superoxide dismutases are the important
antioxidative enzymes that catalyze the dismutation of superoxide
anion into oxygen and hydrogen peroxide. The resultant level of
oxidative stress in formaldehyde-treated lymphocytes was
investigated. The formaldehyde concentrations of 0, 20, 40, 60, 80
and 120μmol/L were treated in human lymphocytes for 12 hours.
After 12 treated hours, the superoxide dismutase activity change was
measured in formaldehyde-treated lymphocytes. The results showed
that the formaldehyde concentrations of 60, 80 and 120μmol/L
significantly decreased superoxide dismutase activities in
lymphocytes (P < 0.05). The change of superoxide dismutase
activity in formaldehyde-treated lymphocytes may be the biomarker
for detect cellular injury, such as damage to DNA, due to
formaldehyde exposure.
", keywords = "Formaldehyde, lymphocytes, superoxide dismutase
activity.", volume = "7", number = "7", pages = "607-3", }
