The dose contributed from thoron (220Rn) and its progeny has been neglected in the dose assessment because of its short half-life (t1/2 = 55.6 s) and generally low concentrations. Recently, concentrations of 220Rn gas and its progeny were found to be pronounced in the traditional residential dwellings in China, on beaches of India and in other countries. Accordingly, we investigated the biological effects of thoron (220Rn) decay products in various mouse organs, succeeding inhalation of thoron gas in BALB/c mouse. We investigated the biological effects upon thoron inhalation on mouse organs with a focus on oxidative stress. These mice were divided into (4 random groups): sham inhalation, thoron inhalation for 1, 4 and 10 days. Various tissues (lung, liver and kidney) were then collected after the time points and subjected to various biochemical analyses. Immediately after inhalation, mouse tissues were excised for gamma spectrometry and 72 h post inhalation for biochemical assays. The gamma spectrometry counts and its subsequent calculation of the equivalent dose showed varied distribution in the lung, liver and kidney. Our results suggest that acute thoron inhalation showed a differential effect on the antioxidant function and exerted pathophysiological alterations via oxidative stress in organs at a higher dose. These findings suggested that thoron inhalation could alter the redox state in organs; however, its characteristics were dependent on the total redox system of the organs as well as the thoron concentration and inhalation time.
Keywords: DNA damage; Organ pathophysiology; Oxidative stress; Redox status; Thoron.
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