RESUMEN
Oncogenic transformed cells represent an in vitro system mimicking early-stage carcinogenesis. These precancerous cells are subject to a selective removal via apoptosis induced by neighbor cells. By modulating the underpinning intercellular signaling mediated by cytokines and reactive oxygen/nitrogen species, ionizing radiation enhances this removal of precancerous cells in vitro, at doses from a few mGy to a few Gy. However, epidemiological data demonstrate that radiation exposure induces cancer, at least above 100 mGy. Mechanistic modeling of the given anti-carcinogenic process explains this discrepancy: The model reproduces in vitro data on apoptosis and its enhancement by radiation. For in vivo-like conditions with signal lifetimes shorter and cell densities higher than in vitro, radiation is predicted to reduce this anti-carcinogenic mechanism. Early-stage lesions that would be turned dormant or completely removed may grow large and escape this control mechanism upon irradiation.
Asunto(s)
Anticarcinógenos/efectos de la radiación , Apoptosis/efectos de la radiación , Transformación Celular Neoplásica/efectos de la radiación , Neoplasias/radioterapia , Apoptosis/fisiología , Línea Celular Transformada , Transformación Celular Neoplásica/patología , Citocinas/farmacología , Humanos , Modelos Biológicos , Radiación Ionizante , Especies Reactivas de Oxígeno/farmacología , Transducción de Señal/efectos de la radiaciónRESUMEN
Understanding the factors that contribute to the degradation of bioactive compounds during microwave treatment is meaningful for the practical application of this novel technology. The influence of microwave power, energy density, temperature, pH value, and initial concentration of anthocyanins (Acys) on the degradation behavior of malvidin-3-glucoside (Mv-3-glu) and malvidin-3,5-diglucoside (Mv-3,5-diglu) was investigated in this study. Results showed that the degradation of both Acys was accelerated with the increase of microwave power, energy density, temperature, pH value, and initial concentration of Acys. The degradation process of both Acys followed the first-order kinetics model (R² > 0.94), whereas the relationship between Acys degradation and energy density fitted to the logistic model well (R² > 0.98). In addition, Mv-3-glu was more susceptible to the microwave treatment than Mv-3,5-diglu. Compared with heating in a 98 ± 2 °C water bath, both Acys degraded more rapidly under microwave treatment at 100 °C, indicating the occurrence of microwave effect. The results provide a guide for the scientific application of microwave treatment.
Asunto(s)
Antocianinas/efectos de la radiación , Antiinflamatorios no Esteroideos/efectos de la radiación , Anticarcinógenos/efectos de la radiación , Glucósidos/efectos de la radiación , Microondas/efectos adversos , Modelos Químicos , Suplementos Dietéticos/efectos de la radiación , Manipulación de Alimentos , Conservación de Alimentos , CinéticaRESUMEN
Retinyl palmitate (RP), a storage form of vitamin A, is frequently used as a cosmetic ingredient, with more than 700 RP-containing cosmetic products on the U.S. market in 2004. There are concerns for the possible genotoxicity and carcinogenicity of RP when it is exposed to sunlight. To evaluate the photomutagenicity of RP in cells when exposed to ultraviolet A (UVA) light, L5178Y/Tk+/- mouse lymphoma cells were treated with different doses of RP alone/or in the presence of UVA light. Treatment of the cells with RP alone at the dose range of 25-100 microg/ml did not increase mutant frequencies (MFs) over the negative control, whereas treatment of cells with 1-25 microg/ml RP under UVA light (82.8 mJ/cm2/min for 30 min) produced a dose-dependent mutation induction. The mean induced MF (392 x 10(-6)) for treatment with 25 microg/ml RP under UVA exposure was about threefold higher than that for UVA alone (122 x 10(-6)), a synergistic effect. To elucidate the underlying mechanism of action, we examined the mutants for loss of heterozygosity (LOH) at four microsatellite loci spanning the entire chromosome 11, on which the Tk gene is located. The mutational spectrum for the RP + UVA treatment was significantly different from the negative control, but not significantly different from UVA exposure alone. Ninety four percent of the mutants from RP + UVA treatment lost the Tk+ allele, and 91% of the deleted sequences extended more than 6 cM in chromosome length, indicating clastogenic events affecting a large segment of the chromosome. These results suggest that RP is photomutagenic in combination with UVA exposure in mouse lymphoma cells, with a clastogenic mode-of-action.