[Photochemical Processes of Cell DNA Damage by UV Radiation of Various Wavelengths: Biological Consequences].

Photochemical reactions in cell DNA are induced in various organisms by solar UV radiation and may lead to a series of biological responses to DNA damage, including apoptosis, mutagenesis, and carcinogenesis. The chemical nature and the amount of DNA lesions depend on the wavelength of UV radiation. UV type B (UVB, 290-320 nm) causes two main lesions, cyclobutane pyrimidine dimers (CPDs) and, with a lower yield, pyrimidine (6-4) pyrimidone photoproducts (6-4PPs). Their formation is a result of direct UVB photon absorption by DNA bases. UV type A (UVA, 320-400 nm) induces only cyclobutane dimers, which most likely arise via triplet-triplet energy transfer (TTET) from cell chromophores to DNA thymine bases. UVA is much more effective than UVB in inducing sensitized oxidative DNA lesions, such as single-strand breaks and oxidized bases. Of the latter, 8-oxo-dihydroguanine (8-oxodG) is the most frequent, being produced in several oxidation processes. Many recent studies reported novel, more detailed information about the molecular mechanisms of the photochemical reactions that underlie the formation of various DNA lesions. The information is mostly summarized and analyzed in the review. Special attention is paid to the oxidation reactions that are initiated by reactive oxygen species (ROS) and radicals generated by potential endogenous photosensitizers, such as pterins, riboflavin, protoporphyrin IX, NADH, and melanin. The review discusses the role that specific DNA photoproducts play in genotoxic processes induced in living systems by UV radiation of various wavelengths, including human skin carcinogenesis.

Estudo dos efeitos metabólicos e redox de dietas intermitentes / Metabolic and redox effects of intermittent fasting

As dietas intermitentes (IF) compreendem ciclos alternados de 24 horas de jejum e alimentação. Como os efeitos de IF sobre o balanço redox não são bem conhecidos, esse trabalho teve por objetivo avaliar os efeitos desta dieta sobre o estado redox de diferentes tecidos de ratos. Após um mês de tratamento, os fígados dos ratos em IF apresentaram um aumento de capacidade respiratória mitocondrial juntamente com níveis elevados de proteínas carboniladas. Verificou-se ainda um aumento em danos oxidativos no cérebro destes animais. IF promoveu significativa proteção contra danos oxidativos no coração, enquanto que não houve alterações no estado redox do músculo esquelético. Os efeitos metabólicos de IF também foram investigados com o intuito de compreender os mecanismos envolvidos com o menor peso e a hiperfagia promovidos por esta intervenção. Observou-se que o menor peso dos ratos submetidos à IF é consequência de um aumento em taxas metabólicas em dias de alimentação somado à oxidação lipídica aumentada durante o jejum. A hiperfagia, por sua vez, é consequencia de elevação nos níveis de neurotransmissores orexigênicos hipotalâmicos, mesmo quando estes animais estão alimentados. Os níveis do neutransmissor TRH também foram modulados por esta dieta, o que pode estar relacionado com as alterações de taxas metabólicas observadas no modelo. Concluímos, portanto, que as dietas intermitentes promovem modificações funcionais no hipotálamo que estão associadas com diferenças no peso corpóreo e no apetite. Além disso, IF afeta o balanço redox de forma tecido específica, levando a um desbalanço oxidativo no fígado e no cérebro e à proteção contra danos oxidativos no coração

Intermittent fasting (IF) is a dietary intervention that comprises 24 hour cycles alternating ad libitum feeding and fasting. We address here the effects of IF on redox state in different tissues, which are still poorly understood. After one month on the diet, IF rats livers presented increased mitochondrial respiratory capacity along with increased levels of protein carbonyls. Surprisingly, IF animals also presented an increase in oxidative damage in the brain. Conversely, IF promoted a substantial protection against oxidative damage in the heart. No difference in redox homeostasis was observed in the skeletal muscle. We also assessed metabolic effects of IF to uncover the mechanisms involved in the lower body mass and loss of feeding control in IF rats. As measured calorimetrically, IF animals presented high metabolic rates during feeding days and increased lipid oxidation on fasting days, which explains the lower body weight. IF-induced overeating was a consequence of increased expression of hypothalamic orexigenic neurotransmitters, even on feeding days. THR levels also were changed, in parallel with the feeding-dependent alterations on metabolic rates. Overall, we find that intermittent fasting promotes functional hypothalamic alterations associated with differences in body weight and appetite. In addition, IF affects redox balance in a tissue-specific manner, leading to redox imbalance in the liver and brain, as well as protection against oxidative damage in the heart

El balance redox en personas expuestas a las radiaciones electromagnéticas (radiaciones no ionizantes) / Redox balance in people exposed to electromagnetic radiations (non-ionizing radiations)

Las ondas electromagnéticas emitidas por campos con frecuencias ultra altas (0,3-3 Ghz) conllevan el peligro de efectos biológicos que pueden convertirse en efectos adversos para la salud. Uno de estos efectos adversos es el desbalance redox con incremento en la producción de radicales libres y la disminución de las defensas antioxidantes. Por tal motivo el objetivo del trabajo consistió en conocer la influencia de las radiaciones electromagnéticas sobre un grupo de personas expuestas y compararla con otro grupo no expuesto tomado como control. Se denota un incremento de la superóxido dismutasa, un incremento de H2O2, una disminución de la capacidad antioxidante total del plasma, un aumento de malondialdehído y no cambios en la concentración de catalasa en los sujetos expuestos. Se concluye que en estos se produce un desbalance redox