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Effects of Radioactivity on Plants and Animals
Published in Michael Pöschl, Leo M. L. Nollet, Radionuclide Concentrations in Food and the Environment, 2006
This process, although not as rapid as the initial ionization event, occurs in the time frame of 10−12 sec. The molecule H2O+ is an ion radical (it is both electrically charged and contains an unpaired electron). It has a short life span (less than 10−10 sec) and decays to form the highly reactive hydroxyl radical (OH·), which has a life span of approximately 10−5 sec. Once these species have been produced, they go on to react chemically with their environment, based on diffusion-controlled reaction kinetics [4].
Translation
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
The R17 complex I was studied exhaustively by Olke C. Uhlenbeck's team in Urbana, Illinois, and further in Boulder, Colorado. They were the first to conduct the entire enzymatic synthesis of 21-nucleotide fragment corresponding to the positions from −17 to +4 of the replicase gene (Krug et al. 1982). By the synthesis, the T4 RNA ligase was used to join shorter oligomers. This sequence was identical with the R17 replicase initiator region and also encompassed the binding domain of the R17 coat protein. The resulting fragment had a secondary structure with the expected thermal stability, and demonstrated the same affinity by the coat binding as the 59-nucleotide fragment isolated from the R17 RNA and described above (Krug et al. 1982). The kinetic and equilibrium properties of the interaction between the 21-nucleotide RNA operator and the R17 coat were studied by the filter retention assay (Carey and Uhlenbeck 1983). The kinetics of the reaction were consistent with the equilibrium association constant and indicated a diffusion-controlled reaction. The temperature dependence of Ka gave ΔH = −19 kcal/mol. This large favorable ΔH was partially offset by a ΔS = −30 cal mol−1 deg−1 to give a ΔG = −11 kcal/mol at 2°C in 0.19 M salt. The binding reaction had a pH optimum centered around pH 8.5, but pH had no effect on the ΔH. While the interaction was insensitive to the type of monovalent cation, the affinity decreased with the lyotropic series among monovalent anions. The ionic strength dependence of Ka revealed that ionic contacts contributed to the interaction. Most of the binding free energy, however, was regarded as a result of nonelectrostatic interactions (Carey and Uhlenbeck 1983).
Beyond Enzyme Kinetics
Published in Clive R. Bagshaw, Biomolecular Kinetics, 2017
The hybridization of short DNA oligomers (10–50 base pairs) must be one of the most widely exploited reactions in molecular biology and is reasonably well understood at the thermodynamic level. Melting temperatures (Tm) can be calculated from the composition of the oligonucleotides with good accuracy [207]. However, the kinetics are more complex. On mixing two complementary single-stranded oligonucleotides, association typically occurs with an apparent second-order rate constant of 106 to 107 M−1 s−1 in the presence of cations to counter the repulsion of the phosphate groups [208–210]. This is two to three orders of magnitude smaller than the expected encounter rate constant for a diffusion-controlled reaction (Section 3.5). Furthermore, the apparent association rate constant becomes smaller with increasing temperature. This negative activation energy is characteristic of the existence of a metastable intermediate [211]. Mechanistically, these observations can be explained by a two-step reaction (Equation 2.39), where an unfavorable collision complex is formed in which only one or two base pairs are present. This intermediate will tend to dissociate, especially at higher temperatures. However, occasionally, a third base pair will form, which allows the remaining bases to pair up rapidly and cooperatively in a zipper-like fashion to give the final stable duplex DNA (Figure 5.8). Essentially, this is a nucleation reaction, where the formation of the first few base pairs is key before the reaction can progress further. Although a minimum of two states are required to explain these data, the kinetic profiles usually appear as a single step because the [DNA] used is normally below the equilibrium constant of the first step (1/K1) and the second step (k+2) is often too fast to measure by stopped-flow methods [209].
NLRP3 inflammasome activation increases brain oxidative stress after transient global cerebral ischemia in rats
Published in International Journal of Neuroscience, 2023
Larissa Silva Joaquim, Lucinéia Gainski Danielski, Sandra Bonfante, Erica Biehl, Khiany Mathias, Tais Denicol, Erick Bagio, Everton Venicius Lanzzarin, Richard Simon Machado, Gabriela Costa Bernades, Jaqueline Generoso, Amanda Della Giustina, Tatiana Barichello, Fabricia Petronilho
Thus, some investigations have focused on oxidative stress markers, such as nitric oxide (NO) [47], after cerebral I/R. NO is a gasotransmitter with imperative role in maintaining cerebrovascular homeostasis [48], but cerebrovascular injury after I/R is associated with exorbitant NO presence and consequent production of RNS [49]. Superoxide anion (O2−) and NO released by activated microglia act as devastating pro-inflammatory mediators in the CNS diseases [50]. More importantly, peroxynitrite (ONOO−), the product of a diffusion-controlled reaction of NO with O2−, is a more potent oxidant specie and is involved in the IS [51]. Additionally, evidence supports that high levels of RNS, particularly NO-derived RNS, are critical for NLRP3 inflammasome activation [52]. RNS also play an important role as evidenced by the fact that both an ONOO− scavenger and NOX2 inhibitor suppressed nigericin-induced caspase-1 activation and IL-1β secretion in human monocytes [53]. Additionally, K+ efflux can be positively regulated by ROS and RNS (e.g. ONOO−) [54]. In this regard, ONOO− formation is responsible for NLRP3 inflammasome activation, favoring oxidative stress and neuroinflammation [52]. Here, N/N concentration, the main NO metabolite, increased after I/R injury in the prefrontal cortex, hippocampus and cortex and the inhibition of NLRP3 reduced the formation of N/N after I/R in the prefrontal cortex and cortex.