China
Africa
Explore chapters and articles related to this topic
Hormesis
Published in T. D. Luckey, Radiation Hormesis, 2020
Hormesis with an electromagnetic focus might include components of various wave motions within a picosecond time frame. An intriguing example is the tunnel diode. At voltages below those where normal diode characteristics are exhibited, the tunnel diode provides a very brief reverse electron flow before the main current becomes established.21
Acute exposure to C60 fullerene damages pulmonary mitochondrial function and mechanics
Published in Nanotoxicology, 2021
Dayene de Assis Fernandes Caldeira, Flávia Muniz Mesquita, Felipe Gomes Pinheiro, Dahienne Ferreira Oliveira, Luis Felipe Silva Oliveira, Jose Hamilton Matheus Nascimento, Christina Maeda Takiya, Leonardo Maciel, Walter Araujo Zin
Our finding of increased production of ROS could be related to the impaired oxygen consumption by ETC experimentally energized with complex I substrates (pyruvate–malate). About 5% of the electrons that flow along the electron transport chain leak into the mitochondrial matrix and form a superoxide anion that is quickly converted into hydrogen peroxide by the enzyme superoxide dismutase and permeates the membrane (Quinlan et al. 2012; Moreno-Sánchez et al. 2013). Interestingly, the pathophysiological relevant sites of ROS generation in the mitochondrial ETC are: (i) the flavin mononucleotide (FMN) group of complex I (where electrons leakage occurs during the reverse electron flow), and (ii) the complex II (Liu, Fiskum, and Schubert 2002; Moreno-Sánchez et al. 2013). However, our study demonstrated that electron leakage did not occur under our experimental conditions. Moreover, our results of pulmonary inflammation could be associated with fullerene C60-induced oxidative stress by mechanisms involving mitochondrial dysfunction, such as NLRP3 inflammasome activation positively regulated by reactive oxygen species (ROS) (Zhou et al. 2011).
Bile acid oxidation by Eggerthella lenta strains C592 and DSM 2243T
Published in Gut Microbes, 2018
Spencer C. Harris, Saravanan Devendran, Celia Méndez- García, Sean M. Mythen, Chris L. Wright, Christopher J. Fields, Alvaro G. Hernandez, Isaac Cann, Phillip B. Hylemon, Jason M. Ridlon
When CDCA was added to an E. lenta sp. strain C592 growth culture, CDCA accounted for only 1.62 ± 0.11% of the total remaining bile acids after 24 hours growth under a N2 atmosphere (0.68 atm) vs. 74.4 ± 2.02% under a H2 atmosphere (0.68 atm) (p < 0.001), indicating that H2 strongly inhibits bile acid oxidation. A similar observation was made with E. lenta DSM 2243 (Figure 6). N2 atmosphere favored the formation of the most oxidized bile acid metabolite, 3,7-dioxocholanoic acid, which represented 47.55 ± 1.71% of the CDCA metabolites in E. lenta C592 vs. 0.38 ± 0.33% under H2 atmosphere (p < 0.001). 7-oxoLCA was the second most abundant metabolite in both strains representing 36.82 ± 0.24% from E. lenta C592 and 52.12 ± 1.92% under N2, compared with 14.03 ± 1.04% and 12.75 ± 0.99%, respectively, under H2 atmosphere. The formation of isoCDCA derivatives (3β-hydroxyl), which requires oxidation of 3α-hydroxyl forming a stable 3-dehydro-intermediate followed by reduction, was essentially ablated under H2. Similar experiments with C. scindens VPI 12708 demonstrate that bile acid 7α-dehydroxylation is not affected by the gas atmosphere (Figure S4). These findings may indicate that E. lenta can utilize hydrogenases and reverse electron flow to generate NADH from H2 and that the gas atmosphere in the gut may be an important regulator of bile acid metabolism by particular intestinal bacteria (Figure 6).
Current evidence for AMPK activation involvement on resveratrol-induced neuroprotection in cerebral ischemia
Published in Nutritional Neuroscience, 2018
Narayana Pineda-Ramírez, Germán Fernando Gutiérrez Aguilar, Mónica Espinoza-Rojo, Penélope Aguilera
There are three specific compounds used ordinarily to evaluate the role of AMPK in experimental models: (1) AICAR (5-aminoimidazole-4-carboxamide ribonucleoside), an activator that mimics the effect of AMP on allosteric activation of AMPK67; (2) Metformin, a drug used to activate AMPK indirectly through inhibition of the mitochondrial respiratory chain complex I in intact cells; by contrast to other inhibitors such as rotenone, it also reduces ROS production by blocking the reverse electron flow68; and (3) Compound C, a non-specific AMPK inhibitor used in cell-based assays; although its IC50 value is of 0.1–0.2 μM, it inhibits other kinases with comparable or superior potency and needs 40 μM to completely inhibit AMPK.69 There are several AMPK like kinases which are activated by LKB1 but are not dependent on AMP, metformin or AICAR.70 This information is useful when conclusions about the role that AMPK plays in specific processes are made.