Categories: glutathione assay Tags: assay, cytosol, from, glutathione, liver, peroxidase, reductase
OXIDATIVE STRESS AND DNA DAMAGE INDUCED BY A DRINKING-WATER CHLORINATION DISINFECTION BYPRODUCT 3-CHLORO-4- … TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS]
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This digital writing is a book article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, publicised by Elsevier in 2006. The article is delivered in HTML info and is acquirable in your Amazon.com Media Library directly after purchase. You crapper analyse it with some scheme browser.
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3-Chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), a liquid gas disinfection byproduct, crapper rush polymer alteration (e.g., change of nucleotides and polymer forsake breaks) and ensuant polymer bushel in vitro. However, the inexplicit mechanism(s) how polymer alteration is evoked by MX is unknown. We hypothesized that MX haw drive oxidative pronounce that leads to polymer alteration in vivo. In the inform study, we unclothed groups of mice to MX at concentrations of 0 (solvent control), 11 (low), 33 (medium) and 99 (high) mg/kg b.w. by azygos intraperitoneal injection. After treating the mice for 3h, we perceived cancellated levels of malondialdehyde (MDA) and glutathione (GSH) to set oxidative pronounce in the direct cells. In addition, we also evaluated polymer alteration using azygos radiophone neaten action (SCGE or Comet assay). We institute that the levels of polymer alteration in every radiophone types were correlated positively with levels of MDA but negatively with levels of GSH (P<0.05 for all). Also, there were perverse correlations between levels of MDA and GSH (r=-0.995 for liver cells, -0.916 for kidney cells, -0.975 for gut cells, respectively; P<0.05 for every but kidney cells). Our findings declare that MX haw rush polymer alteration by the execution of feat cancellated oxidative pronounce as rhythmic by accumulated MDA and attenuated GSH, at small in mice.
Categories: glutathione assay Tags: 3chloro4, byproduct, chlorination, damage, disinfection, drinkingwater, Environmental, induced, Mutagenesis, oxidative, stress, Toxicology
ALTERATION OF INTRACELLULAR GSH LEVELS AND ITS ROLE IN MICROCYSTIN-LR-INDUCED DNA DAMAGE IN HUMAN HEPATOMA HEPG2 CELLS
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This digital writing is a book article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, publicised by Elsevier in 2006. The article is delivered in HTML info and is acquirable in your Amazon.com Media Library directly after purchase. You crapper analyse it with some scheme browser.
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Microcystin-LR (MCLR) is a liver-specific toxin famous as a growth advertizer in empiric animals. Its mechanisms of hepatotoxicity hit been substantially documented; however, the mechanisms of another effects, in portion those attendant to its genotoxicity, are not substantially understood. In our preceding studies, we showed that MCLR-induced polymer forsake breaks are transiently inform and that the alteration is mediated by excited gas species (ROS). In this study, we exhibit that danger of HepG2 cells to non-cytotoxic doses of MCLR-induced time-dependent alterations in the take of intracellular low glutathione (GSH). These comprised a fast initial modification followed by a sloping increase, achievement a peak after 6h of exposure, before backward to the curb take after 8h. During the prototypal 4h, countenance of glutamate-cysteine ligase (GCL), the rate-limiting enzyme of GSH synthesis, increased, indicating an accumulated evaluate of de novo reasoning of GSH. The most essential attending of this study, compounded with the results of our preceding studies is the reciprocity between the instance instruction of alterations of intracellular GSH noesis and the manufacture and leaving of MCLR-induced polymer damage. When the intracellular GSH take was reduced, MCLR-induced polymer alteration was observed to increase. Later, when the take of intracellular GSH was connatural or elevated, newborn polymer alteration was not evoked and existing alteration was repaired. To support the persona of GSH grouping in MCLR-induced genotoxicity, the intracellular GSH take was tempered by pre-treatment with buthionine-(S,R)-sulfoximine (BSO), a limited GSH reasoning inhibitor, and with N-acetylcysteine (NAC), a GSH precursor. Pre-treatment with BSO dramatically accumulated the status of HepG2 cells to MCLR-induced polymer damage, patch pre-treatment with council nearly completely prevented MCLR-induced polymer damage. Thus, intracellular GSH is shown to endeavor a grave persona in the cancellated accumulation against MCLR-induced polymer alteration in HepG2 cells.
Categories: glutathione assay Tags: Alteration, cells, damage, hepatoma, HepG2, human, Intracellular, levels, microcystinLRinduced, role
DNA STRAND BREAKING CAPACITY OF ACRYLAMIDE AND GLYCIDAMIDE IN MAMMALIAN CELLS
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This digital writing is a book article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, publicised by Elsevier in 2005. The article is delivered in HTML info and is acquirable in your Amazon.com Media Library direct after purchase. You crapper analyse it with some scheme browser.
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We compared the polymer harmful powerfulness of acrylamide (AA) and its metabolite glycidamide (GA) in the comet assessment in radiophone systems differing with attitude to species lineage and cytochrome P450-depended monooxygenase (CYP2E1) countenance (V79, Caco-2, direct work hepatocytes). Only after 24h birth in the maximal immersion of AA (6mM) a offense but momentous process in polymer alteration was observed in V79 and Caco-2 cells. In direct work hepatocytes, however, expressing material amounts of CYP2E1, no stimulation of polymer forsake breaks was found. At the modify of the birth instance punctuation (24h), ease 67+/-19% of the CYP2E1 accelerator was perceived by Western blotting. Direct communication with GA resulted in a momentous process in polymer alteration in V79 cells and direct work hepatocytes at concentrations >=100@mM (24h). Caco-2 cells were institute to be inferior sensitive, exhibiting an process in polymer forsake breaks at concentrations >=300@mM GA. These accumulation support the higher genotoxic possibleness of GA compared to AA but also inform that broad countenance of CYP2E1 per se is not needs related with accumulated genotoxicity of AA. We, therefore, investigated whether the intracellular glutathione (GSH) take strength be a grave determinative for the genotoxicity of AA in cells with assorted CYP2E1 status. Depletion of intracellular GSH by dl-buthionine-[S,R]-sulfoxime (BSO) in work hepatocytes and V79 cells resulted in a momentous stimulation of polymer forsake breaks after birth with 1mM AA. However, at higher concentrations (>=1.25mM) a brawny process in cytotoxicity, resulting in a nonindulgent expiration of viability, was observed. In summary, the polymer forsake breaking gist of AA appeared not to be direct correlated with the CYP2E1 position of the cells. Depletion of GSH is related with an process in AA genotoxicity but seems also to advance to a material improvement of cytotoxicity.
DNA forsake breaking power of acrylamide and glycidamide in mammalian cells
Categories: glutathione assay Tags: acrylamide, breaking, capacity, cells, glycidamide, mammalian, strand