Abstract
Cells in vitro or in vivo pre-exposed to low-dose radiation (LDR) or low concentrations of chemical mutagens became more resistant to large-dose radiation-induced DNA or chromosome damage. This was known as radio-adaptive response, for which the exact mechanism was unclear. However, multiple cellular and molecular responses to LDR have been documented, for instance, the induction of some cytokines such as interferon (IFN). Adminstration of exogenous IFN to cultured cells or mice showed marked radio-protection. In the present study, we investigated the in vivo radio-protective effects of extracted human liver RNA (HL-RNA), a known IFN inducer, indirectly to determine the radio-protective action of endogenous IFN. First, mice were administered with 6.25 mg/kg HL-RNA at different times before exposure to radiation and the 24 h pretreatment offered the optimal protective action for HL-RNA on cytogenetic effects in bone marrow cells. When the mice were treated with different concentrations of HL-RNA for 24 h, a wide dose-range (25–100 mg/kg) of HL-RNA resulted in a marked protection from X-ray-induced chromosome aberrations in both bone marrow cells and germ cells. In subsequent experiments, a protective effect of pretreatment with 25 mg/kg HL-RNA for 24 h was also found for radiation-induced micronuclei in polychromatic erythrocytes (PCE), and inhibition of DNA repair ability (unscheduled DNA synthesis, UDS). These results demonstrated that HL-RNA, an IFN inducer, is able to offer significant cytogenetic protection from radiation, implying indirectly that the induction of IFN by LDR may also play a protective role as one of the mechanisms in the induction of the cytogenetic adaptive response.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.