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Showing papers on "Sodium dichromate published in 1985"


Journal Article
TL;DR: The in vivo binding of chromium to whole chromatin, polynucleosomes, DNA, and cytoplasmic RNA-protein fraction from liver and kidney was examined after treatment of rats with sodium dichromate and chromium(III) chloride to find a possible correlation between chromium binding to chromatin and DNA damage.
Abstract: The in vivo binding of chromium to whole chromatin, polynucleosomes, DNA, and cytoplasmic RNA-protein fraction from liver and kidney was examined after treatment of rats with sodium dichromate and chromium(III) chloride. Significant amounts of chromium were bound to DNA and the nonhistone proteins of chromatin and to cytoplasmic RNA-protein fraction. The binding of chromium to the nuclear and cytoplasmic nucleic acid fractions varied considerably, depending on the tissue and the oxidation state of the chromium administered. The level of chromium bound to whole chromatin was greater in the liver than in the kidney after treatment with either chromium compound. Chromium entered the liver and kidney tissues at a slower rate after chromium(III) treatment than after chromium(VI) treatment. At early times after chromium(VI) treatment, more chromium was bound to the liver and kidney chromatin and DNA than after chromium(III) treatment. A much smaller proportion of the chromium bound to chromatin was associated with the DNA after treatment with chromium(III) than after treatment with chromium(VI). However, 40 hr after injection, there was no significant difference in the level of chromium on the DNA from both the liver and kidney of chromium(VI)- and chromium(III)-treated animals. No DNA damage was detected in either liver or kidney nuclei after chromium(III) treatment, using the technique of alkaline elution. A possible correlation between chromium binding to chromatin and DNA damage is discussed.

91 citations


Journal ArticleDOI
TL;DR: The results show that respiratory defence and immunologic functions were stimulated or inhibited depending on dose and time of chromium (VI) inhalation.
Abstract: In inhalation chambers, 5-week-old male Wistar rats of the strain TNO-W-74 were continuously exposed to submicron aerosols of sodium dichromate in concentrations from 25 (low level) to 200 micrograms/m3 Cr (high level). Subacute exposure (28 days) to 25 and 50 micrograms/m3 Cr resulted in "activated" alveolar macrophages with stimulated phagocytic activities, and significantly elevated antibody responses to injected SRBC's. After subchronic (90 days) low level exposure there was a more pronounced effect on activation of the alveolar macrophages, with increased phagocytic activities. However, at high Cr (VI) exposure level (200 microgram/m3), inhibited phagocytic function of the alveolar macrophages was seen. In rats which were exposed to this chromium aerosol concentration for 42 days, the lung clearance of inert iron oxide was reduced significantly. The humoral immune system was still stimulated at subchronic low chromium aerosol concentrations of 100 micrograms/m3, but significantly depressed at 200 micrograms/m3 Cr. These results show that respiratory defence and immunologic functions were stimulated or inhibited depending on dose and time of chromium (VI) inhalation.

81 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: These two short-term tests were effective in detecting the genotoxicity of both direct-acting compounds and procarcinogens and were successfully applied to discriminate the activity of chromium compounds as related to their valence.
Abstract: 5 oil dispersants and a sample of paraffin were devoid of mutagenic activity in the Ames reversion test, with and without S9 mix, using 7 his − S. typhimurium strains (TA1535, TA1537, TA1538, TA97, TA98, TA100, TA102). However, 3 dispersants produced direct DNA damage in E. coli WP2, which was nonrepairable in repair-deficient strains (WP2 uvrA , CM871, TM1080), as shown by two different DNA-repair test procedures. The uvrA excision-repair system was in all cases the most important mechanism involved in repairing the DNA damage produced by oil dispersants, while the combination of uvrA with other genetic defects ( polA, recA, lexA ) decreased the efficiency of the system. The observed genotoxic effects were considerably lowered in the presence of S9 mix containing liver S9 fractions from Aroclortreated rats. The sample of oil dispersant yielding the most pronounced DNA damage in repair-deficient E. coli failed to induce gene sfiA in E. coli (strain PQ37), using the SOS chromotest, or mitotic crossing-over in Saccharomyces cerevisiae (strain D5). The direct toxicity of the oil dispersant to both bacterial and yeast cells was markedly decreased in the presence of rat-liver preparations. These two short-term tests were effective in detecting the genotoxicity of both direct-acting compounds (such as 4-nitroquinoline N -oxide and methyl methanesulfonate) and procarcinogens (such as cyclophosphamide, 2-aminoanthracene and 2-aminofluorene). Moreover, the SOS chromotest was successfully applied to discriminate the activity of chromium compounds as related to their valence (i.e. Cr(VI) genotoxic and Cr(III) inactive). Combination of oil dispersants with Cr(VI) compounds did not affect the direct mutagenicity to S. typhimurium (TA102) of a soluble salt (sodium dichromate) nor did it result in any release of a water-soluble salt (lead chromate), as also confirmed by analytical methods. On the other hand, exposure to sunlight tended to decrease, to a slow rate, the direct genotoxicity of an oil dispersant in the bacterial DNA-repair test.

21 citations


Journal ArticleDOI
TL;DR: In this paper, the solar optical parameters were determined by spectral reflectance measurements and a sol values obtained were around 0.90 and e 373 values in the interval 0.10-0.15.

12 citations


Journal ArticleDOI
TL;DR: Immediate treatment should include urgent induction of emesis, administration of ascorbic acid as an antidote, followed by supportive treatment.
Abstract: Sodium dichromate ingestion in children is uncommon and potentially lethal. The most appropriate management is uncertain because of the lack of sound data contained in the few reports of successfully treated patients. Immediate treatment should include urgent induction of emesis, administration of ascorbic acid as an antidote, followed by supportive treatment.

11 citations


Journal ArticleDOI
01 Nov 1985-Fuel
TL;DR: In this article, two numerical characteristics, Δ(H/C) and potential homocyclic aromatic condensation index (PHAC), were developed to describe the oxidation products, which enabled relationships with commonly used indicators of coal maturation to be discerned by using simple statistical techniques.

7 citations


Patent
16 Oct 1985
TL;DR: In this article, a new anhydrous sodium dichromate in flakes, Na2 Cr2 O7, m.p. 356° C (dec. 400° C) is described, characterized in that it comes in flakes with an area of approx. 1 cm2, thickness 0.5 mm and apparent specific gravity 1.10 (absolute 2.748) at 25° C; it is not deliquescent, nor does it become powdery.
Abstract: A new anhydrous sodium dichromate in flakes, Na2 Cr2 O7, m.p. 356° C. (dec. 400° C.) is described, characterized in that it comes in flakes with an area of approx. 1 cm2, thickness 0.5 mm and apparent specific gravity 1.10 (absolute 2.748) at 25° C.; it is not deliquescent, nor does it become powdery. It is prepared from dihydrate sodium dichromate or aqueous solutions thereof using a new process in two stages, namely (a) evaporation-melting of the dihydrate salt or concentrated aqueous solution at a strictly controlled temperature of around 380° C. and no higher, and (b) flaking of the melted mass obtained thereby, as it is being rapidly cooled to 150°-160° C. The apparatus for carrying out the process is also claimed; said apparatus consisting essentially of a dehydrator-melter oven, a flaker rotating at 10-20 revs per minute and a heat recovery system. The thermic contribution, respectively positive and negative in the two stages, is provided by means of a particular eutectic mixture of melted salts, which melts at 139° C. Said mixture is composed of KNO3 52.2%, NaNO3 7.0%, NaNO2 39.4%, K2 Cr2 O7 1.4%.

6 citations


Journal ArticleDOI
01 Nov 1985-Fuel
TL;DR: In this article, the authors investigated the aromatic structures present in vitrinite concentrates from Australian coals covering a range of rank and found that only 13 relatively simple aromatic carboxylic acids, principally the di- and triacids of benzene, combined in widely different proportions constituted the oxidation products.

4 citations


Patent
18 Jul 1985
TL;DR: In this article, an oxide film is formed on the surface of an Al or Al alloy body to be treated by anodic oxidation, and the body is treated in a pore sealing soln such as an aqueous soln.
Abstract: PURPOSE:To improve the heat resistance of an oxide film formed on the surface of an Al or Al alloy body to be treated by treating the body to seal the pores in the oxide film and by heating it to a specified temp. CONSTITUTION:An oxide film is formed on the surface of an Al or Al alloy body to be treated by anodic oxidation. The body is treated in a pore sealing soln. such as an aqueous soln. of sodium dichromate or deionized boiling water to seal the pores in the oxide film, and it is immediately heated to 140-200 deg.C, especially 170-190 deg.C and held at the temp. for 30-60min, especially 40-50min.

2 citations