Partial contribution of mitochondrial permeability transition to t-butyl hydroperoxide-induced cell death.

Mitochondrial permeability transition (MPT) is thought to determine cell death under oxidative stress. However, MPT inhibitors only partially suppress oxidative stress-induced cell death. Here, we demonstrate that cells in which MPT is inhibited undergo cell death under oxidative stress. When C6 cells were exposed to 250 µM t-butyl hydroperoxide (t-BuOOH), the loss of a membrane potential-sensitive dye (tetramethylrhodamine ethyl ester, TMRE) from mitochondria was observed, indicating mitochondrial depolarization leading to cell death. The fluorescence of calcein entrapped in mitochondria prior to addition of t-BuOOH was significantly decreased to 70% after mitochondrial depolarization. Cyclosporin A suppressed the decrease in mitochondrial calcein fluorescence, but not mitochondrial depolarization. These results show that t-BuOOH induced cell death even when it did not induce MPT. Prior to MPT, lactate production and respiration were hampered. Taken together, these data indicate that the decreased turnover rate of glycolysis and mitochondrial respiration may be as vital as MPT for cell death induced under moderate oxidative stress.

Rotational output and beam quality evaluations for helical tomotherapy with use of a third-party quality assurance tool.

Our aim was to determine whether a third-party quality assurance (QA) tool was suitable for the measurement of rotational output and beam quality in place of on-board detector signals. A Rotational Therapy Phantom 507 (507 Phantom) was used as a QA tool. The rotational output constancy (ROC507) and the beam quality index ([Formula: see text]) were evaluated by analysis of signals from an ion chamber inserted into the 507 Phantom. On-board detector signals were obtained for comparisons with the data from the 507 Phantom. The rotational output (ROC(detector)) and beam quality (corrected cone ratio; CCR) were determined by analysis of on-board detector signals that were generated by irradiation. The tissue phantom ratio at depth 20 and 10 cm (TPR20, 10) was measured with a Farmer-type ionization chamber inserted in a plastic-slab phantom. For rotational output measurement, the correlation coefficient between ROC507 and ROC(detector) values was 0.68 (p < 0.001). ROC507 and ROC(detector) values showed a reduced coefficient of variation after magnetron replacement, which was done during the measurement period. In addition, ROC507 values were reduced significantly along with ROC(detector) values after target replacement (p < 0.001). Regarding the beam quality index, [Formula: see text] showed a change similar to CCR and an increase similar to TPR20, 10 after magnetron/target replacement. This QA tool could check for daily rotational output and detect changes in rotational output and beam quality caused by magnetron or target failure as well as when on-board detector signals were used. Without needing a tomotherapy quality assurance license, we could effectively and quantitatively estimate the rotational output and beam quality at a low cost.

Evaluation of parotid gland function using equivalent cross-relaxation rate imaging applied magnetization transfer effect.

Safe imaging modalities are needed for evaluating parotid gland function. The aim of this study was to validate the utility of a magnetic resonance imaging (MRI) tool, equivalent cross-relaxation rate imaging (ECRI), as a measurement of parotid gland function after chemoradiotherapy. Subjects comprised 18 patients with head-neck cancer who underwent ECRI and salivary gland scintigraphy. First, we calculated ECR values (signal intensity on ECRI), maximum uptake rate (MUR) and washout rate (WOR) from salivary gland scintigraphy data at the parotid glands. Second, we investigated correlations between ECR values and each parameter of MUR (uptake function) and WOR (secretory function) obtained by salivary gland scintigraphy at the parotid gland. Next, we investigated each dose-response for ECR, MUR and WOR at the parotid gland. A correlation was detected between ECR values and MUR in both the pre- (r = -0.55, p < 0.01) and post-treatment (r = -0.50, p < 0.05) groups. A significant post-treatment correlation was detected between the percentage change in ECR values at 3-5 months after chemoradiotherapy and median dose to the parotid gland (Pearson correlation, r = -0.62, p < 0.05). However, no correlations were detected between median dose to the parotid gland and either MUR or WOR. ECRI is a new imaging tool for evaluating the uptake function of the parotid gland after chemoradiotherapy.