Abstract
Cellular RNA prepared from various tissues of mice exposed to ambient levels of nitrogen dioxide (NO 2) for 1 to 20 weeks was examined for evidence of changes in the level of expression of endogenous retrovirus genes. Two strains of mice were used: low retrovirus expressor (Swiss Webster strain) and high retrovirus expressor (AKR strain). Low expressor mice were exposed to 0.8 ± 0.05 ppm and the high expressor mice to 0.3 ± 0.05 ppm NO 2. Among the tissues examined (lung, kidney, thymus, and spleen) of the low expressor mice only the spleen showed a significant elevation of the level of endogenous viral RNA in response to the NO 2 exposure. The elevation did not persist throughout the study; it was detected during the 1st and 18th weeks of exposure, whereas the viral RNA levels were near normal at periods in between. Similarly, the high expressor mice appeared to react to NO 2 exposure with the spleen showing enhanced retrovirus gene expression during the 1st, 8th, 12th, and 15th weeks of exposure. Measurements at the end of the 2nd and 20th weeks of study, however, showed comparable levels in spleens of the exposed and control mice. Although the activity of the virus genes is naturally elevated in the thymic tissue of AKR mice, the levels of viral RNA or the incidence of thymic lymphoma were not significantly altered by exposure to 0.3 ppm NO 2. The observed alterations of genetic expression in the splenic tissue of two different strains of mice, together with the fact that the spleen is closely interrelated with circulating blood components, support the emerging notion that the spleen is a target organ for the effects of inhalation of ambient levels of NO 2.
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.