Journal of Environmental Pathology, Toxicology and Oncology

ISSN for PRINT: 0731-8898

For Online Access

Best Paper Award Selection - Editorial Board Site

2004, Volume23

Issue 1

88 pages

DOI: 10.1615/JEnvPathToxOncol.v23.i1

Issue price - $160.00

Anirban Kumar Mitra
Radiation Biology Division, Bhabha Atomic Research Centre, Trombay, Mumbai, India

Asiti Sarma
Nuclear Science Centre, New Delhi, India

Malini Krishna
Radioprotection and Decontamination Section, Radiation Biology and Health Sciences Division, Bhabha Atomic Research Centre, Mumbai-400085, India

Naresh C. Verma
Radiation Biology Division, Bhabha Atomic Research Centre, Mumbai, Pin. (400 085), India

Heavy ion irradiation of cells is known to increase cytotoxic, mutagenic, and carcinogenic effects. The increased biological effectiveness of these ions is as yet unexplained, except for the fact that, unlike γ-radiation, they result in clustered damage. It is likely that the increased biological effectiveness is a consequence of altered signaling pattern, which in turn may be due to the difference in the nature of damage produced. Gamma irradiation has been known to activate both pro- and anti-apoptotic signaling pathways. Nuclear factor-κB (NF-κB) and extracellular signal regulated kinase (ERK) contribute to the survival of the irradiated cell. Moreover, NF-κB acts as a redox sensor. In the present study, we examined NF-κB and ERK as antiapoptotic factors that could lead to the inhibition of apoptosis and, consequently, to increased mutagenicity. Both these signaling factors show a fluctuation in their levels with time.

DOI: 10.1615/JEnvPathToxOncol.v23.i1.50 Download article, 8 pages

Article price - $35.00

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