[[The movement of rural labor and the establishment of small towns as suggested by factors of production]].
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Agriculture↗
Biomedical subjects
X Shi
Publications and source records attributed to X Shi.
[A problem worthy to be noted by society and parents].
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Asia↗
Effect of temperature and baroreceptor stimulation on reflex venomotor responses.
To investigate the interaction of thermal reflexes and baroreflexes in the control of the peripheral veins, we studied in supine humans the effects of lower body negative pressure (LBNP) and neck suction (NS) on forearm veins at ambient temperatures (Ta) of 18, 28, and 37 degrees C. Forearm venous volume (FVV)-venous pressure (FVP) relations (forearm venous capacitance) on six subjects showed an increase from 18 through 28 to 37 degrees C (P less than 0.001). Heart rate increased (P less than 0.001) and forearm venous capacitance decreased (P less than 0.001) in proportion to the level of LBNP applied from 20 to 50 Torr at all Ta. At 50 Torr LBNP, FVV at 30 cmH2O, FVP decreased from control values of 2.5, 3.8, and 4.4 to 1.6, 2.7, and 3.4 ml/100 ml at 18, 28, and 37 degrees C, respectively. We also studied venomotor responses using the occluded limb technique. Although LBNP caused venoconstriction, NS applied either alone or during LBNP produced no change in venomotor tone. Therefore we concluded that carotid baroreceptors play little role in reflex venomotor adjustments. Since changes in mean arterial and pulse pressures during LBNP did not account for the observed venomotor responses, we concluded that low-pressure baroreceptors initiate significant venoconstrictor reflexes over a wide range of Ta.
Adult↗
[Measures and effectiveness in controlling omission of reports on infant deaths in Shanghai metropolitan areas].
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Asia↗
QSAR with few compounds and many features.
Fitting quantitative structure-activity relationships (QSAR) requires different statistical methodologies and, to some degree, philosophies depending on the "shape" of the data matrix. When few features are used and there are many compounds, it is a reasonable expectation that good feature subset selection may be made and that nonlinearities and nonadditivities can be detected and diagnosed. Where there are many features and few compounds, this is unrealistic. Methods such as ridge regression RR, PLS, and principal component regression PCR, which abjure feature selection and rely on linearity may provide good predictions and fair understanding. We report a development of ridge regression for the underdetermined case by using generalized cross-validation to choose the ridge constant and perform F-tests for additional information. Conventional regression diagnostics can be used in followup to identify nonlinearities and other departures from model. We illustrate the approach with QSAR models of four data sets using calculated molecular descriptors.
Algorithms↗
Generation of free radicals from model lipid hydroperoxides and H2O2 by Co(II) in the presence of cysteinyl and histidyl chelators.
Electron spin resonance spin trapping was utilized to investigate the generation of free radicals from cumene hydroperoxide (cumene-OOH), tert-butyl hydroperoxide (tert-butyl-OOH), and H2O2 at pH 7.2 by Co(II) in the presence of cysteinyl and histidyl chelating agents. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide. Incubation of Co(II) with cumene-OOH or tert-butyl-OOH did not generate any detectable amounts of free radicals. However, in the presence of glutathione, cysteine, penicillamine, or N-acetylcysteine, Co(II) generated cumene-OOH-derived carbon-centered radicals, cumene alkoxyl radicals, and hydroxyl (.OH) radicals. Oxidized glutathione and cystine used instead of reduced glutathione or cysteine did not generate any free radical, indicating an important role of the -SH group in radical generation. While the addition of diethylenetriaminepentaacetic acid (DTPA) prevented radical generation, deferoxamine had only a slightly inhibitory effect. Similar results to those obtained using cumene-OOH were obtained utilizing tert-butyl-OOH in place of cumene-OOH. The yields of free radicals were in the order of glutathione > cysteine > penicillamine > N-acetylcysteine. Incubation of Co(II) with cumene-OOH ort-butyl-OOH in the presence of the histidyl oligopeptide Gly-Gly-His also generated lipid hydroperoxide-derived free radicals, with the yield being comparable to that obtained using thiols. In contrast, histidine, anserine, homocarnosine, or carnosine did not cause any free radical generation from Co(II) and lipid hydroperoxides. Incubation of Co(II) with H2)2 produced only a small amount of .OH radicals.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcysteine↗
Hemoglobin potentiates the production of reactive oxygen species by alveolar macrophages.
The objectives of this investigation were (1) to determine the effects of hemoglobin on the production of reactive oxygen species by activated rat alveolar macrophages, (2) to determine a possible mechanism for these effects, and (3) to determine which part of the hemoglobin molecule is responsible for these effects. Production of reactive oxygen species by phorbol myristate acetate (PMA)-stimulated cells was assessed by measuring luminol-enhanced chemiluminescence (CL). Hemoglobin enhances PMA-stimulated CL in a dose-dependent manner. The effect is maximal at 0.5-1.0 microM hemoglobin where PMA-induced CL is increased by approximately 20-fold. Superoxide anion release from PMA-stimulated cells is not affected by hemoglobin. However, the hemoglobin-induced enhancement of PMA-stimulated CL is inhibited by superoxide dismutase, catalase, dimethylthiourea, or deferoxamine. These results suggest that hydroxyl radical may be formed from hydrogen peroxide which is derived from superoxide anion. Measurements of electron spin resonance spectra following spin trapping of radicals verify that hydroxyl radicals are produced by the cells in the presence of PMA and hemoglobin. The hemoglobin effects appear to require iron in a protoporphyrin complex, because hemin stimulates PMA-induced CL, whereas neither ferrous nor ferric iron has any effect. These findings taken together suggest that hemoglobin can act as a biological Fenton reagent to enhance the production of reactive oxygen species from alveolar macrophages and potentially contribute to lung damage during leakage of blood into the alveolar spaces.
Animals↗
Reactive oxygen species and silica-induced carcinogenesis.
Although silica has recently been designated as a carcinogen, its mechanism of carcinogenesis is not fully understood. Recent studies suggest that free-radical reactions may play an important role in the initiation and progression of cancer. This article summarizes literature on the generation of reactive oxygen species (ROS) directly from silica and from silica-stimulated cells. It also summarizes information concerning the role of ROS in silica-induced DNA damage as well as in silica-induced cell proliferation, including the effects of silica on the activation of nuclear transcription factors, induction of growth factors and oncogene expression, redox regulation of the p53 tumor suppressor gene, induction of apoptosis, and division of damaged cells. Understanding the role of ROS in silica-mediated reactions may help develop therapeutic agents to block silica-induced free radical reactions and thus prevent or attenuate silica-induced carcinogenesis.
Animals↗
Reduction of chromium(VI) and its relationship to carcinogenesis.
Although Cr(VI)-containing compounds are well-documented carcinogens, their mechanism of action is still not well understood. Recent studies have suggested that reduction of Cr(VI) to its lower oxidation states and related free-radical reactions play an important role in carcinogenesis. This article summarizes recent studies on (1) the reduction of Cr(VI) by ascorbate, diol- and thiol-containing molecules, certain flavoenzymes, cell organelles, intact cells, and whole animals; (2) free-radical production with emphasis on hydroxy radical generation via Fenton or Haber-Weiss type reactions; and (3) free-radical-induced cellular damage, such as DNA strand breaks, hydroxylation of 2'-deoxyguanosine, and activation of nuclear transcription factor kappa B.
Animals↗
The role of superoxide radical in TNF-alpha induced NF-kappaB activation.
Electron spin resonable (ESR) spin trapping with 5-(diethioxyphosphoyl)-5-methyl-1-pyrroline N-oxide (DEPMPO) was utilized to investigate the generation of oxygen free radicals from macrophages stimulated by tumor necrosis factor-alpha (TNF-alpha). TNF-alpha stimulated macrophages generated hydroxyl (*OH) and superoxide anion (O2*-) radicals. Incubation of TNF-alpha with macrophages resulted in an activation of DNA binding activity of the nuclear transcription factor NF-kappaB. Superoxide dismutase (SOD), but not catalase or sodium formate, inhibited this NF-kappaB activation, suggesting that O2*- rather than H2O2 or *OH, radicals play the most critical role in this induction. beta-Nicotinamide adenine dinucleotide phosphate (NADPH) did not affect the NF-kappaB activation, while allopurinol, an inhibitor of xanthine oxidase, repressed it, suggesting that xanthine/xanthine oxidase, and not NADPH dependent oxidase, may be a source of O2*- radicals which induce NF-kappaB activation. 02*- is generated via reduction of molecular oxygen by xanthine and xanthine oxidase, as demonstrated by the oxygen consumption assay. The results indicate that TNF-alpha induces oxygen radical generation from macrophages. 02*- seems to play a key role in TNF-alpha-induced NF-kappaB activation in macrophages. Xanthine and xanthine oxidase appears to be a source of O2*- radicals responsible for TNF-alpha-induced NF-kappaB activation.
Animals↗
Vanadium(IV) causes 2'-deoxyguanosine hydroxylation and deoxyribonucleic acid damage via free radical reactions.
Vanadium(IV) caused molecular oxygen dependent 2'-deoxyguanosine (dG) hydroxylation to form 8-hydroxyl-2'-deoxyguanosine (8-OHdG). During a 15-minute incubation of 1.0 mM dG and 1.0 mM VOSO4 (vanadium(IV)) in phosphate buffer solution (pH 7.4) at room temperature under ambient air, dG was converted to 8-OHdG with a yield of about 0.31 percent. Catalase and formate inhibited the 8-OHdG formation while superoxide dismutase enhanced it. Diethylenetriaminepentaacetic acid (DTPA) and deferoxamine blocked the 8-OHdG formation. Incubation of vanadium(IV) with dG in argon did not generate any significant amount of 8-OHdG, indicating the role of molecular oxygen in the mechanism of vanadium(IV)-induced dG hydroxylation. Vanadium(IV) also caused molecular oxygen dependent deoxyribonucleic acid (DNA) strand breaks in a pattern similar to that observed for dG hydroxylation. Reaction of vanadium(IV) with H2O2 generated OH radicals, which were inhibited by DTPA and deferoxamine. Incubation of vanadium(IV) with dG or with DNA in the presence of H2O2 resulted in an enhanced 8-OHdG formation and substantial DNA strand breaks. Reaction of vanadium(IV) with t-butyl hydroperoxide generated hydroperoxide-derived free radicals, which caused 8-OHdG formation from dG and DNA strand breaks.
Chelating Agents↗
Low frequency electron paramagnetic resonance investigation on metabolism of chromium (VI) by whole live mice.
Detection of Cr(V) in the reduction of Cr(VI) by whole live mice and its characterization were carried out by low frequency electron paramagnetic resonance (EPR). Intravenous injection of Cr(VI) to mice generated Cr(V). The Cr(V) was found predominantly in the liver with a small amount in the blood. Liver homogenates from Cr(VI) treated mice generated essentially the same Cr(V) spectrum as that obtained from the whole live mice. This Cr(V) species was identified to be a Cr(V)-nicotinamide adenine dinucleotide (NAD) (P)H complex with an oxygen bond to Cr(V). Pretreatment of the mice with ascorbic acid and glutathione reduced the Cr(V) formation, while pretreatment with reduced nicotinamide adenine dinucleotide (NADH) enhanced it. Metal chelators, ethylenediaminetetraacetic acid (EDTA), 1,10-phenanthroline, and diethylenetriaminepentaacetic acid (DTPA) inhibited the intensity of the Cr(V) signal. The results suggest that Cr(V) generated in the whole body of a live animal is a Cr(V)-NAD(P)H complex and NAD(P)H/flavoenzymes and not glutathione or ascorbate as the major one-electron Cr(VI) reductant responsible for observed formation of Cr(V)-NAD(P)H complex in vivo.
Animals↗
Chromium (IV)-mediated fenton-like reaction causes DNA damage: implication to genotoxicity of chromate.
This paper describes our deoxyribonucleic acid (DNA) damage and Fenton activity studies on Cr(IV) that were undertaken to examine a role of Cr(IV) in the biochemical mechanism of genotoxicity of Cr(VI) compounds. A Cr(IV)-containing compound, a Cr(IV)-ester, was synthesized and used as the first model compound for Cr(IV) studies. Electron spin resonance measurements demonstrated that in the presence of H2O2, this Cr(IV) compound acts as a potent Fenton-like reagent, i.e., it generates OH radical and a Cr(V) species (g = 1.9787) via: Cr(IV) + H2O2-->Cr(V) + OH + OH-. Measurements of OH yield as a function of H2O2 concentration showed that Cr(IV) is more potent than Cr(V) in generating OH. DNA damage assays demonstrate that Cr(IV) and the Cr(IV)/H2O2-generated OH radical can cause DNA strand breaks. The DNA damage caused by OH radical can be effectively blocked by OH radical scavengers. These results thus constitute the first direct evidence for DNA damage by Cr(IV) and Cr(IV)-mediated Fenton-like reaction and support the conjecture that Cr(IV) plays a significant role in the biochemical mechanism of the genotoxic reactions of Cr(VI) compounds and that this effect can be modulated by suitable antiradical agents.
Animals↗
Efficacy of taurine based compounds as hydroxyl radical scavengers in silica induced peroxidation.
While it is widely believed that taurine may play an important role in protecting cells against toxic injury by functioning as an antioxidant, there is a lack of evidence to support this hypothesis. In this study, electron spin resonance (ESR) was used to investigate the reaction of taurine and hypotaurine with hydroxyl radicals (.OH). The Fenton reaction (Fe(II) + H2O2-->Fe(III) + .OH + OH-) and the Cr(V)-mediated Fenton-like reaction (Cr(V) + H2O2-->Cr(VI) + .OH + OH-) were used as sources of .OH radicals. The results show that hypotaurine but not taurine effectively scavenges .OH radicals with a reaction rate constant of k = 1.6 x 10(10) M-1s-1. That is comparable with other efficient .OH radical scavengers. The effect of taurine and hypotaurine on silica-induced lipid peroxidation was evaluated using linoleic acid as a model lipid. Hypotaurine, but not taurine, caused a significant inhibition of silica-induced lipid peroxidation. The results show that hypotaurine is an excellent antioxidant and appears to have the potential for being a therapeutic agent against silica-induced lung injury.
Antioxidants↗
Vanadium (IV) formation in the reduction of vanadate by glutathione reductase/NADPH and the role of molecular oxygen.
Experimental evidence documenting the formation of a relatively stable V(IV) species appears to be important with regard to the biochemical mechanism of reduction of vanadate by enzymatic systems. The present study demonstrates that a mixture of vanadate and glutathione reductase/nicotinamide-adenine-dinucleotide phosphate (NADPH), in phosphate (pH 7.2) buffer generates V(IV) under ambient conditions. Once formed, V(IV) does not rapidly autoxidize so as to defy detection by electron spin resonance (ESR) spectroscopy. The aerobic environment was guaranteed by preparing reaction mixtures in well stirred, wide mouth, standard test tubes in air over a period of 50 minutes, and by making ESR measurements in nuclear magnetic resonance (NMR) sample tubes as well as oxygen-permeable Teflon tubes. The V(IV) ESR signal intensity was found to increase linearly with time elapsed after reaction initiation. The linear growth of the V(IV) species also shows that this species is fairly stable, over a period of at least 50 minutes. Similar V(IV) stability data were obtained from VOSO4, a model compound as a source of V(IV). The results obtained in the present study demonstrated that V(IV) can be generated in the reduction of V(IV) by glutathione reductase in the presence of NADPH under aerobic condition.
Electron Spin Resonance Spectroscopy↗
Simple, at-site detection of diethylene glycol/ethylene glycol contamination of glycerin and glycerin-based raw materials by thin-layer chromatography.
This paper describes a rapid, inexpensive thin-layer chromatographic (TLC) method that separates diethylene glycol (DEG) from glycerin and other glycols. Studies with collaborating laboratories of the World Health Organization have shown that about 6% DEG in glycerin and about 2% DEG in acetaminophen (paracetamol) elixirs may be detected by direct visual inspection of the developed TLC sheets. Staining the sheet permits detection of DEG at less than 0.1%. The method costs less than $1.00 per test and takes 20 min by visual inspection, longer when staining is required. The visual method can be performed without laboratory facilities by personnel having little previous training. Samples testing positive by the visual method can be submitted to a laboratory for confirmation and quantitation of DEG.
Acetaminophen↗
Role of hydroxyl radical in silica-induced NF-kappa B activation in macrophages.
Nuclear transcription factor kappa B (NF-kappa B) is a multiprotein complex that regulates a variety of genes important for immunity and inflammation. The present study investigates the silica-induced activation of this transcription factor in mouse macrophage cell line RAW 264.7 cells, the role of free radical reactions in the mechanism of the activation, and its possible inhibition. Tetrandrine, a benzylisoquinoline alkaloid, which has been used as an antifibrotic drug to treat the lesions of silicosis and has been characterized as a hydroxyl radical (.OH) scavenger, inhibited the NF-kappa B activation induced by silica, lipopolysaccharide (LPS), and phorbol 12-myristate 13-acetate (PMA). Catalase, metal chelator, deferoxamine, and the silanol group (SiOH) blocker, poly(2-vinylpyridine-N-oxide) (PVPNO), also inhibited silica-induced NF-kappa B activation. Electron spin resonance (ESR) spin trapping measurements show that both deferoxamine and PVPNO decreased silica-mediated .OH radical generation from H2O2. It is shown that Fe(II) and not Fe(III) is able to cause NF-kappa B activation. The antioxidant, ascorbate, attenuated the NF-kappa B activation induced by silica but not by LPS. The .OH radical scavenger, sodium formate, inhibited NF-kappa B activation induced by silica but had only a minor effect on NF-kappa B activation induced by LPS. The results indicate that silica-mediated free radical generation via the Fenton or Fenton-like reaction (M(n)+ + H2O2-->M(n + 1)+ + OH- + .OH) and silanol groups on the silica surface play an important role in silica-induced NF-kappa B activation.
Alkaloids↗