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Sodium dichromate

About: Sodium dichromate is a research topic. Over the lifetime, 421 publications have been published within this topic receiving 6202 citations. The topic is also known as: Disodium salt & sodium bichromate.


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Journal ArticleDOI
TL;DR: Investigation of multigene expression in the liver and lung of rats receiving intratracheal instillations of sodium dichromate triggered a variety of defense processes in the lung, contributing to the understanding of chromium toxicology and providing a further mechanistic support to the involvement of thresholds in chromium(VI) carcinogenesis.
Abstract: Multigene-expression analysis provides a formidable tool for evaluating cellular functions, under either physiological or pathological conditions, and for assessing their modulation by exogenous agents. We investigated multigene expression in the liver and lung of rats receiving intratracheal instillations of sodium dichromate for 3 consecutive days. Nylon membrane cDNA arrays were hybridized with standardized amounts of 32P-labeled probes, and the results were normalized by making reference to housekeeping genes. The basal expression of 52 of 216 tested genes was 2.1–11.1 times higher in the liver than in the lung of control rats. No alteration of gene expression occurred in the liver of chromium(VI)-treated rats, consistent with the fact that this metal species, being reduced upstream, can exert effects only locally but not at a distance from the respiratory tract. In contrast, the expression of 56 genes was increased 2.1 to 3.0 times in the lung as an early response to chromium(VI) administration. The altered genes are involved in the metabolic reduction of chromium(VI) and in a variety of interconnected functions, such as multidrug resistance and stress response, protein and DNA repair mechanisms, signal transduction pathways, apoptosis, and cell-cycle modulation. Thus, short-term treatment with chromium(VI) by intratracheal administration triggered a variety of defense processes in the lung. Although the use of selected genes does not provide an exhaustive picture of overall gene expression, these findings contribute to our understanding of chromium toxicology and provide a further mechanistic support to the involvement of thresholds in chromium(VI) carcinogenesis. © 2002 Wiley-Liss, Inc.

41 citations

Journal Article
TL;DR: Findings indicate that, in addition to already recognized detoxification mechanisms operating outside target cells, specific and inducible chromium-reducing pathways, mediating threshold phenomena in chromium carcinogenesis, do also occur in the intracellular environment.
Abstract: The mutagenicity of sodium dichromate in the Ames test was decreased as a consequence of chromium(VI) reduction by tissue postmitochondrial (S-9 or S-12) fractions from untreated rats with the following rank of efficiency: liver; kidney; and lung. The effects of lung preparations were significantly enhanced following the intratracheal administration of high doses (0.25 mg/kg) of dichromate itself, 5 times per week for 4 weeks (i.e., 20 fractionated instillations). No changes were conversely detected following single weekly doses of 1.25 mg/kg for the same period (i.e., four cumulative instillations). The local stimulation of chromium(VI) metabolism was also confirmed by testing the mutagenicity of calcium chromate and chromium trioxide, whereas the metabolism of a number of other activatable or deactivatable mutagens was not significantly affected by intratracheal treatment with chromium(VI). Of three enzyme inducers injected i.p. which modified the spectral properties and/or concentration of cytochromes P-450 in liver and lung microsomes, only Aroclor 1254 proved to stimulate chromium(VI) metabolism in lung cells. In liver cells, Aroclor 1254 and to a lower extent phenobarbital induced chromium(VI) reduction, while 3-methylcholanthrene was ineffective. Pretreatment of rats with these three compounds resulted in a selective induction of the metabolic activation of promutagens [benzo(a)pyrene and its trans-7,8-diol, 2-aminofluorene, aflatoxin B1] and of the metabolic deactivation of direct-acting mutagens {2-methoxy-6-chloro-9-[3-(2-chloroethyl)-aminopropylamino]acridine·2HCl, epichlorohydrin, 4-nitroquinolino-N-oxide} by S-12 and microsomal fractions. These findings indicate that, in addition to already recognized detoxification mechanisms operating outside target cells (26), specific and inducible chromium-reducing pathways, mediating threshold phenomena in chromium carcinogenesis, do also occur in the intracellular environment.

37 citations

Journal ArticleDOI
TL;DR: The results of this study indicate that fluorometric analysis of DNA unwinding (FADU) in peripheral lymphocytes might be a convenient method of measuring an important biological effect of chromium in occupationally-exposed workers.
Abstract: 1 Incubation of human lymphocytes with sodium dichromate (CrVI) at 37°C for 3 h resulted in a dose-dependent increase in DNA strand breaks without concurrent cytotoxicity. In contrast, chromium acetate hydroxide (CrIII) failed to induce DNA strand breaks at sub-cytotoxic concentrations.2 DNA strand breaks were also detected in the peripheral lymphocytes of Wistar rats, 24 h after intratracheal instillation of sodium dichromate (1.3 and 2.5 mg kg-1 ). Instillation of chromium acetate hydroxide (up to 21.8 mg kg -1) failed to induce DNA strand breaks in peripheral lymphocytes. In accord with previous studies, hexavalent chromium was found to be more readily absorbed from the lungs into the peripheral blood than chromium in its trivalent form.3 The results of this study indicate that fluorometric analysis of DNA unwinding (FADU) in peripheral lymphocytes might be a convenient method of measuring an important biological effect of chromium in occupationally-exposed workers.

37 citations

Journal ArticleDOI
TL;DR: Results are consistent with previous data, showing that hexavalent chromium and either benzo[a]pyrene or cigarette smoke condensate behave antagonistically in in vitro mutagenicity test systems and that the chromium reducing capacity of human pulmonary alveolar macrophages and peripheral lung parenchyma is enhanced in smokers.
Abstract: A combination of tobacco smoking with certain agents has been shown to exert synergistic carcinogenic effects. On the other hand, antagonism betweeen smoke and other pulmonary carcinogens has also been documented by both epidemiological and experimental data. In spite of a very large number of studies carried out for decades in workers exposed to hexavalent chromium, the influence of smoking habits on lung carcinogenesis induced by this metal has not been clarified. For this reason, we performed two studies evaluating clastogenic effects in rodents. In the first one, BDF(1) mice were exposed whole-body to mainstream cigarette smoke for 5 days and, on the last day, they received an i.p. injection of potassium dichromate. In the second study, Sprague-Dawley rats were exposed whole-body to environmental cigarette smoke for 18 consecutive days and for the same period of time they received daily intra-tracheal instillations of sodium dichromate. Individually, the two hexavalent chromium salts and cigarette smoke, either mainstream or environmental, enhanced the frequency of micronuclei in bone marrow polychromatic erythrocytes of both mice and rats. Moreover, individual exposure to either environmental cigarette smoke or sodium dichromate enhanced the frequency of micronuclei and multiple nuclei in pulmonary alveolar macrophages of rats. In both studies, combined exposure to cigarette smoke and hexavalent chromium produced less than additive clastogenic effects. These results are consistent with our previous data, showing that hexavalent chromium and either benzo[a]pyrene or cigarette smoke condensate behave antagonistically in in vitro mutagenicity test systems and that the chromium reducing capacity of human pulmonary alveolar macrophages and peripheral lung parenchyma is enhanced in smokers. Taken together, in the absence of any epidemiological evidence, these findings rule out any occurrence of synergism between cigarette smoke and hexavalent chromium, at least in certain stages of the carcinogenesis process.

37 citations

Journal ArticleDOI
TL;DR: Aqueous polymerization of 3-chloroaniline (mCA) was studied using sodium dichromate as oxidant in the presence of hydrochloric acid in this article.
Abstract: Aqueous polymerization of 3-chloroaniline (mCA) was studied using sodium dichromate as oxidant in the presence of hydrochloric acid The effect of hydrochloric acid, sodium dichromate and monomer concentration on the polymerization rate, specific viscosity of the obtained polymer and ac conductivity was investigated The initial and overall reaction rates increase with increasing hydrochloric acid concentration or sodium dichromate concentration, but decrease with increasing monomer concentration The specific viscosity values (η sp ) increase with increasing hydrochloric acid concentration or monomer concentration, which means that the molecular weight of the polymer samples increases accordingly On the contrary, the molecular weight decreases with increasing sodium dichromate concentration The highest ac conductivity value of the obtained polymer was found for 00255 moll -1 of Na 2 Cr 2 O 7 , 08 moll -1 HCl and 00956 moll -1 monomer concentration in the reaction medium The order of the polymerization reaction with respect to hydrochloric acid, Na 2 Cr 2 O 7 and monomer concentration was found to be 10, 09 and 075, respectively The apparent activation energy (E a ) for this polymerization system was found to be 13674 x 10 4 mol -1 The obtained poly(3-chloroaniline) was characterized by UV-visible, IR and 1 H NMR spectroscopy X-ray diffraction analysis and electron microscopy studies were carried out Thermogravimetric analysis (TGA) and differential thermal analysis (DTA) results were used to confirm the structure

37 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20211
20201
201916
201817
20178
201617