Dimethylsulfoxide increases the survival and lysosomal stability of mouse peritoneal macrophages exposed to low-LET ionizing radiation and/or ionic iron in culture.

Reactive oxygen-derived free radicals form excessively during irradiation of biological structures, but also normally in many cellular oxidative processes, albeit in small amounts. Unless scavenged by protective mechanisms, such radicals may induce peroxidation of polyunsaturated fatty acids resulting in membrane damage. The process may be catalysed to a considerable extent by transitional metals with the capacity to form redox systems, such as Fe3+ in equilibrium Fe2+. In the present study, it is shown that radiation by X-rays and/or exposure to ionic iron (Fe3+) causes decreased survival in parallel with lysosomal labilization of cultured mouse peritoneal macrophages (MPMs). The latter event was demonstrated as a reduced capacity of lysosomes in living MPMs to retain acridine orange during photo-oxidative stress caused by continuous exposure to blue light of short wavelength. The effects of X-irradiation, and/or lysosomal iron-loading, could be counteracted by the addition of the .OH-scavenging drug dimethylsulfoxide (DMSO) to the cell culture medium. The findings suggest that X-irradiation may damage certain sensitive G0 cells, such as Kupffer cells, serous cells of salivary glands and old macrophages, which normally have substantial concentrations of metals within their vacuolar apparatus, possibly by lysosomal damage involving .OH-mediated lipid peroxidation.