670 nanometer light treatment attenuates dioxin toxicity in the developing chick embryo.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an acutely toxic anthropogenic chemical. Treatment with a red to near-infrared (630-1000 nm) light-emitting diode (LED) attenuates the toxicant-induced oxidative stress and energy deficit in neuronal cell culture. For this study, fertile chicken (Gallus gallus) eggs were injected once at the start of incubation with sunflower oil vehicle or 200 pg TCDD/g egg (200 parts per trillion), an environmentally relevant dose. Daily LED treatment after TCDD exposure reduced embryonic mortality by 47%. LED treatment of TCDD-exposed eggs also decreased the hepatic oxidized-to-reduced glutathione ratio by 88%. Activities of other hepatic indicators of oxidative stress, such as glutathione reductase and catalase, were increased after LED treatment of TCDD-exposed eggs. Our study demonstrates that 670 nm phototherapy can mitigate the oxidative stress and energy deficit resulting from developmental exposure to TCDD while reducing TCDD-induced embryo mortality. Moreover, LED treatment restores hepatic enzyme activities to control levels in TCDD-exposed embryos. The effective attenuation of TCDD-induced embryo toxicity by LED treatment could extend to mitigating the effects of other teratogens that induce oxidative and energy stress.

Green tea catechins protect rats from microwave-induced oxidative damage to heart tissue.

We investigated the effects of green tea catechin on oxidative damage in microwave-exposed rats. The microwave-exposed rats received one of three diets: catechin-free (MW-0C), 0.25% catechin (MW-0.25C), or 0.5% catechin (MW-0.5C). Rats were sacrificed 6 days after microwave irradiation (2.45 GHz, 15 minutes). Cytochrome P(450) levels in the MW-0C group was increased by 85% compared with normal, but was 11% and 14% lower in the MW-0.25C and MW-0.5C groups than in the MW-0C group. NADPH-cytochrome P(450) reductase activity in the MW-0C group was increased by 29%, compared with the normal group, but was significantly less in the MW-0.25C and MW-0.5C groups. Superoxide dismutase activity in the MW-0C group was decreased by 34%, compared with the normal group, but in the MW-0.25C and MW-0.5C groups was 19% and 25% higher. The activity of glutathione peroxidase in the MW-0C group was decreased by 28% but remained near normal with catechin supplements. Superoxide radical concentrations in the MW-0C group were increased by 35%, compared with the normal group. However, superoxide radicals in the MW-0.25C and MW-0.5C groups were 11% and 12% lower, respectively, compared with the MW-0C group. Microwave irradiation significantly increased levels of thiobarbituric acid-reactive substances, carbonyl values, and lipofuscin contents, but green tea catechin partially overcame the effects of the microwave irradiation. In conclusion, the mixed function oxidase system was activated, the formation of superoxide radical, lipid peroxide, oxidized protein, and lipofuscin was increased, and the antioxidative defense system was weakened in heart tissue of microwave-exposed rats, but the oxidative damage was significantly reduced by catechin supplementation.

[The effect of the prophylactic use of benzonal on the cytochrome P-450 content of the liver in irradiated rats]. / Vliianie profilakticheskogo primeneniia benzonala na soderzhanie tsitokhroma P-450 v pecheni obluchennykh krys.

The rats (100 mg/kg, once a day, per os, during 3 days) were administered suspension of benzonal in starch gel before irradiation of 12 Gy. Induced and uninduced rats were irradiated on the following day after stopping benzonal administration and were decapitated at 10, 12, 15 and 21 o'clock during the first and second day after irradiation and also on the fourth day (day of mass death of irradiated rats). It has been established that irradiation changes the dynamics of cytochrome P-450 concentration in microsomal fraction of rat liver. The essential decrease of the content of cytochrome on the second day after irradiation was accompanied by intensification of the process of its inactivation, but stoichiometry between the decrease of P-450 and the increase of cytochrome P-420 was not observed. The high inducing and stabilizing effects of benzonal on cytochrome P-450 and on the liver persisted. In comparison with irradiation the unfavourable effect of benzonal on immunocompetent organs (thymus, spleen) was not found.