ABSTRACT
Sonochemistry in a thin fluid layer has advantages of no visible cavitation, no turbulence, negligible temperature changes (â²1 °C), low power transducers, and transmissibility (sound pressure amplification) of â³106. Unlike sonochemistry in semi-infinite fluids, resonance and so constructive interference of sound pressure can be established in thin layers. Constructive interference enables substantial amplification of sound pressure at solid fluid interfaces. Fluid properties of sound velocity and attenuation, oscillator input frequency, and thin fluid layer thickness couple to established resonance in underdamped conditions. In thin layer sonochemistry (TLS), thin layers are established where ultrasonic wavelength and oscillator-interface separation are comparable, about a centimeter in water. Solution of a one dimensional wave equation identifies explicit relationships between the system parameters required to establish resonance and constructive interference in a thin layer.
ABSTRACT
The hypothesis that mitochondrial dysfunction and increased superoxide levels in thymocytes over expressing Bax (Lck-Bax1 and Lck-Bax38&1) contributes to lymphomagenesis after low-dose radiation was tested. Lck-Bax1 single-transgenic and Lck-Bax38&1 double-transgenic mice were exposed to single whole-body doses of 10 or 100 cGy of (137)Cs or iron ions (1,000 MeV/n, 150 keV/µm) or silicon ions (300 MeV/n, 67 keV/µm). A 10 cGy dose of (137)Cs significantly increased the incidence and onset of thymic lymphomas in female Lck-Bax1 mice. In Lck-Bax38&1 mice, a 100 cGy dose of high-LET iron ions caused a significant dose dependent acceleration of lymphomagenesis in both males and females that was not seen with silicon ions. To determine the contribution of mitochondrial oxidative metabolism, Lck-Bax38&1 over expressing mice were crossed with knockouts of the mitochondrial protein deacetylase, Sirtuin 3 (Sirt3), which regulates superoxide metabolism. Sirt3(-/-)/Lck-Bax38&1 mice demonstrated significant increases in thymocyte superoxide levels and acceleration of lymphomagenesis (P < 0.001). These results show that lymphomagenesis in Bax over expressing animals is enhanced by radiation exposure in both an LET and gender dependent fashion. These findings support the hypothesis that mitochondrial dysfunction leads to increased superoxide levels and accelerates lymphomagenesis in Lck-Bax transgenic mice.
