DNA Fluorescence

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Femtosecond fluorescence studies of DNA/RNA constituents

International audienceIn this overview, femtosecond fluorescence studies of various DNA constituents are presented, ranging from the monomeric chromophores to different model helices. In order to interpret the experimental results in terms of fundamental processes on the molecular scale they are discussed in the light of recent theoretical calculations. The ultrafast fluorescence decay observed for the monomers is explained by the involvement of highly efficient conical intersections (CI) between the first singlet excited state and the ground state. For the model helices, the picture is more complex, but fluorescence anisotropy data reveal collective effects

Assessing solvent effects on the singlet excited state lifetime of uracil derivatives: a femtosecond fluorescence upconversion study in alcohols and D2O

The excited state lifetimes of uracil, thymine and 5-fluorouracil have been measured using femtosecond UV fluorescence upconversion in various protic and aprotic polar solvents. The fastest decays are observed in acetonitrile and the slowest in aqueous solution while those observed in alcohols are intermediate. No direct correlation with macroscopic solvent parameters such as polarity or viscosity is found, but hydrogen bonding is one key factor affecting the fluorescence decay. It is proposed that the solvent modulates the relative energy of two close-lying electronically excited states, the bright ΠΠ and the dark nΠ states. This relative energy gap controls the non-radiative relaxation of the ΠΠ state through a conical intersection close to the Frank-Condon region competing with the ultrafast internal conversion to the ground state. In addition, an inverse isotope effect is observed in D2O where the decays are faster than in H2O

Altered thermoregulatory responses to clonidine in streptozotocin-diabetic rats

1 The effects of streptozotocin (STZ) treatment on alpha(2)-adrenoceptor regulation of body temperature were studied by monitoring the response of colonic temperature to administration of clonidine. 2 A dose-dependent fall in colonic temperature occurred in control rats given clonidine challenge (0.05-2.0 mg kg(-1), s.c.); this response was inhibited by prior administration of either yohimbine or idazoxan (2 mg kg(-1), s.c.) but not by the peripherally-acting alpha(2)-adrenoceptor antagonist L-659,066 (10 mg kg(-1), s.c.). 3 In rats treated with STZ (65 mg kg(-1), i.v.) administration of clonidine elicited a dose-independent hyperthermia (circa 1 degrees C.); this effect was unaltered by prior administration of yohimbine or idazoxan. 4 Naloxone (5 mg kg(-1), s.c.) elicited a small fall in temperature (< 1 degrees C.) in both control and STZ-treated rats; naloxone pretreatment did not alter the temperature response to clonidine in either group. 5 Nicotinic acid (10 mg kg(-1), s.c.) caused a similar small elevation in temperature in both groups. 6 Administration of replacement insulin to STZ-treated rats maintained weight gain and low blood glucose while the thermoregulatory response to clonidine slowly reverted to normal. 7 These results show that altered central temperature control is an element of the generalised abnormality of alpha(2)-receptor function induced by STZ

Electronically excited states in DNA studied by fluorescence spectroscopy

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